UNITED STATES DISTRICT COURT

SOUTHERN DISTRICT OF OHIO 

WESTERN DIVISION 

MELANIE BECKEMEYER,

Plaintiff, 

v.

GELCO CORPORATION, etc.,

Defendant.

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CASE NO. 1:17-cv-00695

JUDGE BARRETT

AFFIDAVIT OF ANDREW SAXON, 

M.D.

I, Andrew Saxon, M.D., having been duly sworn do here hereby swear, affirm, depose and 

state as follows:

1. Background education, experience, and training relevant to expertise in this case.

I am a licensed physician in the State of California specializing in the area of Clinical 

Immunology & Allergy. I am the founder and emeritus chief of the Division of Clinical 

Immunology and Allergy at the UCLA School of Medicine, Los Angeles, California. I am 

currently a Professor of Medicine at the David Geffen School of Medicine at UCLA.

I received my medical degree from Harvard Medical School in Boston, Massachusetts, in 1972. I 

completed my residency in internal medicine at Harbor General Hospital in Los Angeles, 

California, in 1975, and my post-doctoral training in immunology in the Department of 

Microbiology and Immunology at the UCLA School of Medicine in 1977. I am a licensed 

physician in California through the National Board of Medical Examiners. I am board certified in 

(1) Internal Medicine by the American Board of Internal Medicine, (2) Allergy and Immunology 

by the American Board of Allergy and Immunology, and (3) Diagnostic Laboratory Immunology 

by the American Board of Diagnostic Laboratory Immunology. I founded the Division of 

Clinical Immunology and Allergy in the Department of Medicine at UCLA in 1977 and served 

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as its Chairman for 30 years. I also founded the UCLA Asthma, Allergy, and Immunologic 

Disease Center and served as Director until the time of my retirement. I have published over 190 

scientific papers in peer-reviewed journals in the field of immunology and I provide many 

editorial/review services for such journals including being Editor in Chief of Clinical 

Immunology, the official journal of the Clinical Immunology Society for over a decade. I also 

have served on peer-review funding committees for the National Institutes of Health and other 

organizations as well as chair the Allergy/Asthma section of the Immune Tolerance Network, a 

major undertaking by the National Institutes of Health and private institutions to discover true 

cures for immune mediated disorders. 

I am a co-author of the American College of Occupational & Environment Medicine (ACOEM) 

original Position Statement entitled: Adverse Human Health Effects Associated with Molds in 

the Indoor Environment that appeared in 2002. ACOEM represents more than 6,000 physicians 

and other health care professionals and is the nation's largest medical society of individuals 

specializing in the field of occupational and environmental medicine. I am also a co-author of the 

American Academy of Allergy Asthma and Immunology’s (AAAAI) official Position statement 

entitled “The Health Effects of Molds” which appeared in 2006. The AAAAI, with over 5000 

members, is the nation’s largest medical subspecialty society specifically dealing with the 

allergic and immune aspects of mold exposures.

Further elaboration of my professional background, prior publications and credentials is given in 

the attached true and correct copy of my curriculum vitae and bibliography (Exhibit “1”). 

2. Data/material reviewed and relied upon in forming opinions.

A. The basis of my testimony includes my education, clinical and basic science training, 

experience, and review of both basic and clinical studies regarding humans and the 

immune system. This includes basic studies performed in the test tube and in animals 

regarding mold and related substances, my own research in human and animal immune 

reactivity, review of the exhibits, depositions and opinions of identified plaintiff experts, 

my extensive reading in the areas of immunology which includes allergy, autoimmunity, 

cancer of the immune system (lymphomas), and related areas, and my clinical experience 

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including the diagnosis and management of patients with immunologically related 

disorders.

B. Included in this is extensive analysis of the literature relating to mold/fungal related 

illness in humans including the Institute of Medicine’s 2004 Publication “Damp indoor 

spaces and Health”, the American College of Medical Toxicology’s Statement in Support 

of the Institute of Medicine’s report and the 2009 World Health Organization (2009) 

“Guidelines for Indoor Air Quality: Dampness and Mould.” I am also relying upon the 

2017 Association of Scientific Medical Societies guideline, “Medical diagnostics for 

indoor mold exposure, the Position Statement of the American College of Occupational 

and Environmental Medicine promulgated by the Society in 2011 and the 2006 Position 

Statement of the American Academy of Allergy, Asthma and Immunology, Asthma and 

Immunology 

C. I am also relying upon my analysis of the case-specific materials provided to me. This 

includes:

C1. Medical records of the plaintiff Melanie Ann Beckemeyer PharmD from the 

following sources that span the timeframe March 2001 through July 2018.

• Allergy and Asthma Specialty Group. 

• Bernstein Allergy Group. 

• Bethesda Alcohol and Drug Treatment (no records) 

• Huber personalized medicine (Dr. Gray Huber, Integrative Medicine)

• Kroger Little Clinic.

• Liberty Urgent Care. 

• Dr. Harold T. Pretorius. 

• Plaintiff produced 2315 pages of medical documents that include the records of 

Dr. Craig P. Cleveland.

• Blue Ash Family Medicine

• Report of Richard Sexton, PhD of April 2017.

C2. Environmental records

• The Report of Jeremy Porter, PMP dated 11.6.18

• Report from Ecostratum dated 7.25.18 for vehicle testing on 7.9.18 

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C3. Legal Documents

• Complaint filed in this matter.

• Discovery responses filed in this matter

• Depositions of Ms. Melanie Beckemeyer, PharmD. dated 9.27.18 and 11.5.18

• Expert Report of Dr. Scott McMahon in Beckemeyer vs. GELCO 8.31.18

• Expert Report of Dr. Scott McMahon in Fleming v Baker 3.29.17 

• Deposition Testimony of Dr. Scott McMahon in Fleming v Baker 4.7.17 

• Depositions of Scott W. McMahon in Courcelle v. CW NOLA PROPERTIES 

dated 8.18.17 and 5.18.18 

• Declaration Of Scott W. Mc Mahon, MD in Courcelle v. CW NOLA Properties 

Dated 8.15.17

• United States District Court Western District of Washington At Seattle, Court 

order 16356136 dated 8.13.15 in Haneet Kumar, et al., v. Williams Portfolio 7, 

Inc.

3. The basis for my opinions.

The basis of my opinions in this in this case includes my; education, training in basic sciences and 

medicine, experience in general as board-certified specialist in internal medicine, allergy and 

immunology, and diagnostic laboratory immunology and as specifically related to mold and 

mycotoxin exposure, review. It also include my analysis of published peer reviewed and accepted 

literature on the effects of molds and mycotoxins on a broad range of mammalian species including 

humans, general knowledge of the adverse effects of chemicals, bacteria, molds, and toxins on 

mammalian species including humans, and records reviewed in this case as outlined in item #2

above.

4. Overview of mold.

Mold and mold spores (reproductive parts released by molds) are ubiquitous in the air and soil in all 

environments and settings. Molds fill every ecological niche on earth with the types and levels of 

specific molds varying with climatic conditions. Molds grow best in warm, damp, and humid 

conditions, and spread and reproduce by making spores. Molds serve a critical role in the 

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recycling of organic materials without which life on this planet could not be sustained. Estimates of 

the number of mold species range from tens of thousands to a hundred thousand or more. 

Mycotoxins are small non-volatile (i.e. not gaseous) chemicals that are byproducts produced by a 

limited number of mold species and are only produced by those molds under certain conditions, 

i.e. they are not constitutively produced. For example, of the over 500 species in the Genus 

Aspergillus, less than 20 produce its major mycotoxin, aflatoxin. Various mycotoxins in low 

levels are present throughout the food chain due to mold growing on crops. 

5. Mechanism of adverse effects from mold and mold byproducts. 

Adverse health effects from mold and their byproducts occur via three main mechanisms: 

Immune, Infectious and Irritant/Toxic. Each of these can be addressed in terms of whether Ms. 

Beckemeyer had/has evidence for an adverse health effect from mold.

A. Immune effects: There are three immune mediated diseases related to molds.

First is typical inhalant “allergy” that causes allergic rhinitis and allergic asthma and 

occurs in genetically predisposed persons who make up about 40% of the population. 

These allergic airway symptoms are due to the result of the production of IgE (allergic) 

antibodies to ubiquitous aeroallergens such as pollens, animal dander, dust mites or 

mold spores. Allergy to mold occurs in about 10% of the population. The other two 

forms of immune adverse health effect from exposure to mold or mold byproducts are 

rare conditions known as allergic bronchopulmonary aspergillosis (ABPA) and 

hypersensitivity pneumonitis in which there is an overly strong immune response in the 

lung to the harmless mold spores that lead to a pneumonia -like picture.

Whether Ms. Beckemeyer has an allergy to mold among other allergies to inhalants is 

unclear from the data in her records (discussed below). Even if she does, such an allergy 

would not account the vast spectrum of her symptoms nor their persistence. There is no 

indication of Ms. Beckemeyer having ABPA or hypersensitivity pneumonitis.

B. Infection: Molds commonly cause superficial infections such as toenail or skin infections 

(ringworm). Four unusual molds in specific outdoor geographic regions cause serious 

infections – primarily pneumonias. However, in profoundly immunocompromised 

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persons, e.g. those on chemotherapy or following bone marrow transplantation, a host of 

common molds can cause serious infections. None of these mold infection issues relate 

to one’s indoor residence or vehicle.

Ms. Beckemeyer has had no mold infections. In fact, the records do not even reflect that 

she has had problems with common superficial mold infections such as toenail or skin 

infections. I would add that any oral or vaginal candida infections she may have had were

due to a yeast, Candida albicans that is not a mold. That yeast is resident on normal 

mucosal surfaces in humans but overgrows to become an infection under a variety of 

circumstances unrelated to ambient environmental conditions.

C. i. Irritant effects: 

Irritant effects from mold can result from inhalation of a very large concentration of mold 

particulates in the air wherein the spores essentially become nuisance dust. Levels in the 

millions of spores/m3 or more would be required for this effect, levels far beyond 

anything found in the vehicle in question. Additionally, in high enough concentrations, 

mold derived volatile organic compounds (VOCs), e.g. gasses that smell and give rise to 

the musty odor associated with mold, can cause local irritant effects, usually of the wet 

membranes of the eye, nose and mouth. However, VOC irritant effects generally occur at 

levels hundreds to thousands of times higher than the odor threshold. Furthermore, even 

if a person had had some local irritant effects from VOCs, albeit there is no data to 

support that supposition, such effects would have been transient by definition, and would 

have disappeared within a week or two of Ms. Beckemeyer no longer being in the vehicle 

in question.

ii. Toxic effects: Toxic effects from inhalation of airborne mold spores in a residential 

setting or a motor vehicle essentially does not occur. This is simply a result of dose 

considerations; i.e. i.) the number of spores a person can inhale, ii.) the toxicity of 

mycotoxins on molar basis, iii.) the maximum amount of mycotoxin per spore (Kelman 

BJ, et al. Int J Toxicol. 23:3-10, 2004,), iv.) the half-life of mycotoxins in humans, and 

v.) the no observed effect level (NOEL) for even the most potent mycotoxins (Hardin 

BD, et al. J. Toxicol. Environ. Health A. 72:585-98, 2009. The calculations from these 

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studies suggests that even under the worst extreme scenario (all mold spores making the 

most potent known mycotoxin, inhalation of maximum amount 24/7, all spores breathed 

deposited and 100% of toxin absorbed) for an adult, it would take between 30,000 to 

>1,000,000 spores/m3 of these spores to have an adverse health effect. Compare that to 

the level of spores found by the Plaintiff’s CIH in the vehicle air in 2018 - the 

airborne/respirable levels had a total 1300 spores/m3 with the majority were harmless 

mushroom spores, i.e. basidiospores. Of the mold spores found in the air, only those of 

Chaetomium (27 spores/m3) are associated with mycotoxin production. Thus the level of 

potential mycotoxin producing spores in the vehicle when tested was thousands of times 

below that at which any toxin related adverse health effect might occur.

As opposed in inhalation, ingestion of mycotoxins in food is a daily occurrence as 

various mycotoxin-producing molds grows on foodstuffs, e.g. peanuts, cereals, cheese 

etc., during their production. Indeed, the FDA and European Union has established limits 

for certain mycotoxin levels in foods. The level of mycotoxins in human food is generally 

quite low and of no health concern. However, there are occasionally outbreaks of 

mycotoxin poisoning in populations when starving persons have little option but to eat

highly spoiled food.

Given the factors discussed above in this section, it is not tenable to propose more likely 

than not that irritancy or toxicity resulting from inhalation of mold spores or their 

byproducts in the air from the vehicle in question as causing Ms. Beckemeyer’s 

symptomatology.

Overall, the generally accepted mechanisms for mold and/or mold byproduct induced adverse 

health effects are not quantitatively or qualitatively relevant to Ms. Beckemeyer’s primary 

medical issues, i.e. her complaints do not even potentially relate to the generally accepted

mechanisms of mold induced adverse health effects other than possibly some mild upper 

airway allergy. 

6. Medical issues that Ms. Berkemeyer had/has as related to her complaints in this matter.

Hypertension - high blood pressure with secondary cognitive issues secondary to small vessel 

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ischemic changes. Ms. Beckemeyer has had high blood pressure since at least 2001 and has been 

maintained on long-term anti-hypertensive medication (Irbesartan most recently). Common side 

effects of Irbesartan include dizziness, fatigue, indigestion, diarrhea and heartburn. An MRI of 

her brain on 6.13.17 showed “microangiopathic white matter disease consistent with chronic 

small vessel ischemia, most often seen in manifestation of hypertensive atherosclerosis or 

metabolic factors.” There was also mild right greater than left hippocampal atrophy that 

potentially may correlate with memory symptoms possibly related to early manifestation of mild 

cognitive impairment syndrome. 

Ms. Beckemeyer has long-standing hypertension with underlying microvascular brain changes 

resulting in a mild impairment of certain cognitive functions, a very common scenario in a 63-

year-old person. Another factor driving in Ms. Beckemeyer’s cognitive complaints is her 

response to anxiety/stress as discussed below.

Anxiety, Panic Attacks and Depression with Somatic Symptom Disorder. Ms. Beckemeyer 

records show that she has had problems with depression, anxiety and panic attacks since 

September of 2011, long before the alleged exposure in this case. At that time, she reported she 

felt that “she cannot complete tasks that require organization and higher levels of cognition in a 

reasonable amount of time due to ongoing anxiety.” She was begun on an anti-depressant

Celexa and was on it through 7.1.16. By mid-2017, Ms. Beckemeyer had developed a whole 

panoply of ongoing symptoms that she felt were related to her exposure to the vehicle in question 

which had ended in September 2016. The symptoms she reported included disturbed sleep, 

fatigue, joint pain/swelling, bladder problems, buzzing/ringing/ear pain, blurry vision, 

disorientation, forgetfulness, loss of libido, unexplained hair loss, vertigo, confusion, difficulty 

with concentration, and swollen glands. She endorsed mood swings/irritability/depression at that 

time as well. 

Ms. Beckemeyer has a generalized anxiety disorder with panic attacks and major depressive 

illness. Notably, when anxious in the past prior to the alleged exposure, she reported cognitive 

symptoms very similar to what she reports now. Her long standing anxiety/mood issues color 

and magnify her symptoms, e.g. fatigue from medications, cognitive changes etc. as well drive 

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such symptoms on their own as such mood issues do in all patients. Ms. Beckemeyer appears to 

have developed a somatic symptom disorder focused on her belief about the injury she received 

from her mold exposure in the vehicle in question. 

Treatment with thyroid hormone. Ms. Beckemeyer has been on thyroid hormone replacement 

medication for many years for unclear reasons. Ms. Beckemeyer’s medical records also show 

that in 2017 she was taking too much thyroid hormone as documented by her very low TSH.

If Ms. Beckemeyer actually does have underlying thyroid disease, which is not evident, it was 

pre-existing and any thyroid issues she may have are not related to exposure to mold, mold 

byproducts or ambient bacteria. Overtreatment with thyroid hormone as documented in 2017 will 

have made her hypertension and her anxiety worse.

Vertigo/disequilibrium/dizziness. Ms. Beckemeyer reports she first had problems with vertigo 

and disequilibrium when she was diagnosed with Meniere’s disease in her 30s. On 9.18.15, Ms. 

Beckemeyer saw her primary care physician complaining of ear pressure and being off balance 

that she described as feeling “swimmy.” She was treated for presumed eustachian tube 

dysfunction. On 9.29.15, Ms. Beckemeyer was seen in urgent care complaining of problems 

with wooziness and vertigo. All this was before the alleged exposure. Then in September of 

2016, she complained of increasing light-headedness and dizziness. Over the ensuing months, 

she had an extensive work up for this including a neuro-otology consultation and no specific 

etiology was found for her complaints of light-headedness and dizziness. 

Ms. Beckemeyer’s more recent complaints of feeling dizzy and lightheaded are most likely a 

manifestation of both her microvascular CNS disease that is secondary to her long standing 

hypertension and her long standing anxiety/stress. 

Upper Respiratory and external ocular symptoms: Ms. Beckemeyer saw an allergist in 2001and 

reported that she had had “allergies” for more than 10 years, clearly long predating her alleged 

mold exposure. Ms. Beckemeyer had allergy testing in 2004 but the test records are incomplete

and uninterpretable. Ms. Beckemeyer had epicutaneous allergy testing on 12.27.16 with only the 

molds Epicoccum and Fusarium recorded as “positive” at 3+ but there is no reading scale for

these tests nor was there a record of the necessary positive (histamine) and negative (saline) 

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control results, which makes them open to question. 

The accessible data are uninterpretable as to whether Ms. Beckemeyer is an allergic (atopic) 

person with allergic rhinitis and allergic conjunctivitis given the problematic test results. Ms. 

Beckemeyer does not have asthma, allergic or otherwise. I would not rely upon the available 

allergy test results to make or exclude a diagnosis of inhalant allergy. This could be resolved by 

Ms. Beckemeyer undergoing reliable allergy blood testing done with the ImmunoCap II or 

equivalent third generation allergy blood testing. Even if Ms. Beckemeyer is an allergic subject 

and the epicutaneous testing is presumed to be accurate, the only allergens identified by this

testing were Epicoccum and Fusarium. These were not found in the air in the vehicle and any

exposure to these in the vehicle in question would have been far less than her exposure from air 

outside her vehicle as discussed in Mr. Porter’s report. 

7. Use of Differential Diagnosis to establishing general and specific causation and “Chronic 

Immune Response Syndrome” or “CIRS.”

A. Differential Diagnosis: Differential diagnosis is the medical parallel of the scientific 

method in which one makes a hypothesis, tests that hypothesis experimentally and then 

rejects or accepts the hypothesis. The “differential diagnosis” is a list of likely generally 

accepted medical conditions, given the evidence in hand, with the working diagnosis 

(hypothesis as to what is wrong with the patient) being the most likely choice based on the 

currently available data. The physician then gathers valid scientific data (additional history, 

physical findings and/or laboratory tests to confirm or exclude that leading diagnosis. 

On page 18 of his report, Dr. McMahon alleges he applies “differential diagnosis” to arrive at 

his final diagnostic impression of Ms. Beckemeyer having “Chronic Immune Response 

Syndrome” or “CIRS” as the overarching cause of her multitude of complaints. However, the 

record in this matter clearly demonstrates that Dr. McMahon is not using differential 

diagnosis in a valid or acceptable fashion. Thus while he claims to exclude other appropriate 

causes before reaching his conclusion, this is not the case. A cogent example of Dr. 

McMahon’s failure to use differential diagnosis appropriately is Dr. McMahon’s dismissal of

hypertension as playing a role in Ms. Beckemeyer’s symptoms. However, her testing shows 

changes indicative of microangiopathic changes in the brain that are common in hypertension 

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and that is generally accepted to cause in mild cognitive impairment. Instead, Dr. McMahon 

ascribes her neurocognitive issues to “CIRS” Another cogent example is Dr. McMahon’s 

failure to appropriately consider Ms. Beckemeyer’s pre-existing and long standing 

generalized anxiety disorder and depression in the genesis of her multiple somatic 

complaints. Generalized anxiety disorder and depression are the two most common forms of 

psychiatric illness in our populations. These disorders commonly give rise to multiple 

somatic symptoms as had been reported by Ms. Beckemeyer five years before her alleged 

exposure. Dr. McMahon again simply ascribes her multiple somatic symptoms to “CIRS”, a 

concept that is not-generally accepted.

Thus Dr. McMahon, while ignoring/dismissing appropriate diagnoses, focuses with laser-like 

certainly on a single all-encompassing not-generally accepted pseudo-diagnosis of CIRS. In 

doing so, Dr. McMahon is not performing differential diagnosis as it is generally accepted in 

medicine. By not following the accepted procedure of differential diagnosis, Dr. McMahon 

comes to conclusions that cannot be relied upon in making his diagnosis of so-called “CIRS”. 

Dr. McMahon says that there is no other single entity other than CIRS that could be 

responsible for Ms. Beckemeyer’s entire myriad of complaints. This proposition is based on 

a false premise; one need not have a single true pathophysiologic disease that encompasses 

all of a patient’s medical issues. Indeed, as discussed earlier in Section 6, Ms. Beckemeyer 

has a number of distinct medical issues, each of which needs to be addressed individually. 

Such a set of different disease processes is typical for 60-year-old individuals.

B. CIRS is not a generally accepted medical condition. The lack of validity of the CIRS as a 

valid medical entity is discussed at length in section IIID of my report (Alternative/fringe 

health care and pseudo-diagnosis of Chronic Inflammatory Response Syndrome, aka “CIRS”, 

Exhibit 3). Briefly, CIRS was invented by a former practicing family physician, Dr. Richie 

Shoemaker. Much of Dr. McMahon report is simply a recitation of the ideas put forth by Dr. 

Shoemaker who for years has been marketing himself and his “patent pending” diagnosis of 

CIRS (United States Patent Application Publication, Pub. No.: US 2014/0046143 A1 

Shoemaker et al., Pub. Date: Feb. 13, 2014, Methods For Diagnosing, Treating, And 

Monitoring Chronic Inflammatory Response Syndrome). This alleged condition that Dr. 

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McMahon currently calls Chronic Immune Response Syndrome or CIRS is not a generally 

accepted entity in the medical community. CIRS is a diagnosis that is unique to Dr. 

Shoemaker and his followers such as Dr. McMahon.

As proposed by Dr. Shoemaker and regurgitated by Dr. McMahon, neither of whom has had 

any formal post graduate education or training in immunology, clinical immunology or 

internal medicine, CIRS is an sustained uncontrolled activation of the innate immune system

due to indoor and only indoor exposure to any of a host of potential microbes/microbial 

products. Additionally, they propose that exposure to such microbes/microbial products in 

the future will lead to enhanced exacerbations of subjects’ CIRS. The claim that CIRS is a 

self- sustaining reaction of the innate immune system is a fatally flawed idea that is in direct 

conflict with what is known about the human innate immune response. The battery of tests 

Dr. McMahon uses to support his diagnosis of CIRS are not generally accepted methodology 

for any purpose in clinical medicine much less for the purpose for which he employs them. 

Dr McMahon’s claim there is no detectable lower limit for an exposure that can induce CIRS 

and that immune responses in CIRS and in immunology in general fail to follow dose 

response relationships is profoundly mistaken and in direct contrast what is known. All 

medicine including toxicology and immunology involve a dose response. Additionally, the 

claim by Dr. McMahon and other CIRS proponents that CIRS only occurs with indoor 

exposure is completely illogical. The literature that Dr. McMahon cites as actually 

supporting his opinions regarding CIRS has been generated by Drs. Mahan, Shoemaker and 

their colleagues while true experts in the relevant fields do not generally accept their work as 

reliable. Dr. McMahon’s belief that CIRS can explain everything that troubles Ms. 

Beckemeyer (or anyone else) is based on the fact the hypothetical construct of CIRS that has 

no boundaries. As a result, the rubric of CIRS, such as it is, can be applied to any person to 

explain all alleged issues, i.e. is all-encompassing, and becomes meaningless it does not

represent a separately definable disease process.

Thus, we have Dr. Scott McMahon, a pediatrician in Roswell, New Mexico, reporting that he 

has seen hundreds of patients who he has diagnosed with CIRS, an alleged immune mediated 

disorder from indoor (and only “indoor”) exposure to mold/dampness. Yet no certified 

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clinical immunologist has ever vetted this diagnosis. So is there really an epidemic of CIRS 

in Roswell, New Mexico? Or is Dr. McMahon, by using “differential diagnosis” in a way 

that is generally not accepted, the cause of this “CIRS epidemic?” 

8. General causation

As discussed earlier in Section 5, mold and/or mold byproducts and dampness related organisms 

can cause a limited known adverse health outcomes/medical issues. However, those generally 

accepted medical effects are not the primary health effects at issue here. At issue in this matter is 

whether mold/mold byproducts and/or dampness related organisms cause 1) non-infectious 

neurological conditions including cognitive impairment, 2) generalized somatic symptoms, e.g. 

fatigue, and/or 3) dizziness/vertigo. The reliable medical literature clearly does not support such 

conclusions. This is nicely summarized in the analyses of the Institute of Medicine (IOM), “Damp 

indoor spaces and Health” (Exec summary Table ES-1 and ES2, Exhibit “2”), the World Health 

Organization “Guidelines for Indoor Air Quality: Dampness and Mould.” and the Association of 

Scientific Medical Societies Guideline publication. None of those authoritative documents found 

even an association between mold or dampness exposure and neurological or generalized 

somatic symptoms (or a host of other health outcomes.) Indeed the IOM found “Inadequate or 

Insufficient Evidence to Determine Whether an Association Exists” for these endpoints. This is in 

contrast to respiratory symptoms where there was “Sufficient Evidence of an Association” though 

the IOM did not feel the data reached the level of “Sufficient Evidence of a Causal Relationship.”

9. Specific causation

Given that there is no basis for general causation for mold, mold byproducts and/or dampness 

related organisms with non-infectious adverse health outcomes except an association for respiratory 

outcomes, specific causation of Ms. Beckemeyer’s non-respiratory issues is moot. Furthermore, 

there are well-accepted causal relationships between her known medical conditions (discussed in 

Section 6) and her complaints. In terms of Ms. Beckemeyer’s respiratory complaints and her 

alleged exposure in 2016, specific causation cannot be established to a reasonable degree of 

medical probability given the lack of valid data in that regard both in terms of the diagnosis of 

allergy and the potential exposures as discussed in Section 6 and Section 10. To propose that Ms. 

Beckemeyer had respiratory symptoms based on alleged exposures in 2016 would be purely 

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speculative. Furthermore, even if Ms. Beckemeyer were to have had some increased respiratory 

symptoms related to 2016 alleged exposure, those symptoms would have been resolved within 

weeks of terminating the alleged exposure.

10. Exposure data

The relevant metric for potential human exposure to mold/mold byproducts and subsequent dose 

calculations is sampling of respirable air. While testing for molds and their byproducts on 

surfaces in a vehicle or home or inside walls may have relevance for remediation efforts, there is 

no way to determine or even estimate the levels of human exposure from such sources and to 

attempt to do so is speculation and not generally accepted methodology for assessing human 

exposure. Similarly, the respirable air sampling must be in a relevant timeframe in terms of when 

the individual was in the location sampled. One cannot sample locations months or years after 

the individual was there and say what was present when the subject was there.

There are no data regarding mold or other microbial materials in vehicle in question during Ms. 

Beckemeyer’s period of use in 2016 much less any data that the amounts were at a level sufficient 

to cause an adverse human health effect. It is impossible to try to derive a valid opinion as to Ms. 

Beckemeyer’s vehicular exposure based on data obtained twenty-two months or later after her last

known use. Yet this is what Dr. McMahon has inappropriately done. He has no scientific basis for 

opining about the mold levels in the vehicle while Plaintiff used it in 2016. Dr. McMahon forms an 

invalid opinion based on data from 2018 testing data and the Plaintiff’s subjective report of 

symptoms during her use in 2016. Defining exposure based on symptoms as Dr. McMahon has 

done is known as “backwards toxicology”, a classic error made by those with no real expert 

knowledge of toxicology. Dr. McMahon’s attempt to “reverse extrapolate” the presence of mold 

and/or mold levels in the vehicle is fatally flawed as it is not based on accepted methodology for 

determining specific causation and as a result his opinions in this regard are invalid and cannot be 

relied upon.

11. Conclusion

It is my opinion to a reasonable degree of medical probability, based upon the records and 

documents available to me, that there is no valid objective evidence to support Plaintiff’s allegation 

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Exhibit 1

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Andrew Saxon, M.D.

Professor of Medicine President, Secretary, & Founder

Chief Emeritus Sixal Incorporated 

Clinical Immunology/Allergy

Department of Medicine Board of Directors, PADI Foundation

UCLA School of Medicine

52-221 Center for the Health Sciences Advisory Board, Summit Street Medical

Los Angeles, CA 90095-1690

Tel: (310) 367-9736 Fax: (310) 206-8622 Scientific Advisory Board, Stellar Biotech.

Email: asaxon@mednet.ucla.edu

EDUCATION:

o Graduate, Deerfield Academy, Deerfield, Massachusetts, 1964

Cum Laude Society, 1963, 1964

Bausch and Lomb Science Award, 1964

o A.B., Anthropology, Dartmouth College, Hanover, New Hampshire, 1968

Phi Beta Kappa, 1968

A.B. Magna Cum Laude

Distinction in Anthropology

Founding Fathers Scholar and Scholarship

o Archaeology/Anthropology (First Class Honors), University of Otago

Dunedin, New Zealand, 1967

o B.M.S., Dartmouth Medical School, Hanover, New Hampshire, 1970

Dean's Medal as First in Class

o M.D., Harvard Medical School, Boston, Massachusetts, 1972

Boylston Society, 1971 - 1972

POSTGRADUATE TRAINING:

o Intern, Straight Medicine, Harbor General Hospital

Los Angeles, California, 1972 - 1973

Outstanding Medical Intern Award

o Resident, Internal Medicine, Harbor General Hospital

Los Angeles, California, 1973 - 1975

o Postdoctoral Scholar in Immunology

Department of Microbiology and Immunology

UCLA School of Medicine

Los Angeles, California, 1975 - 1977

CERTIFICATION AND LICENSING:

o National Board of Medical Examiners (#126793), June 1973

o Licentiate (#G24948), State of California, July 1973

o Diplomate American Board of Internal Medicine (#49823), June 1975

o Diplomate American Board of Allergy and Immunology (#1967), October 1979

o Diplomate American Board of Diagnostic Laboratory Immunology (#0134), October 1990

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PUBLICATIONS

o Approximately 190 peer-reviewed research publications 

PATENTS

o Approximately 10 related to development of agents for the manipulation of the human immune 

response. Examples follow:

• “Fusion Molecules and Methods for Treatment of Immune Disease” •US patent 7,265,208, 

7,534,440 Issued April 19, 2009.

• “Modified Fusion Molecules for Treatment of Allergic Disease”. US application 11/050,113, PCT

application 06/03562

PROFESSIONAL APPOINTMENTS:

o Professor of Medicine Emeritus (rehire), Department of Medicine, UCLA School of Medicine, 2006.

o Executive Director, UCLA Food and Drug Allergy Care Center, 2010 - 2016

o Chief Scientific Officer, Tunitas Therapeutics, 2008 - present

o Scientific Advisory Board, Stellar Biotechnology, 2010 – present, Chairman 2010- 2014

o Professor of Medicine, Department of Medicine, UCLA School of Medicine, 1984 – present.

o Chief, Division of Clinical Immunology/Allergy, UCLA School of Medicine, 1978 – 2006.

o Associate, UCLA Molecular Biology Institute, 1985 – 2013.

o Member, UCLA Jonsson Comprehensive Cancer Center, 1983 – 2006, Associate 2106- present.

o Associate Professor of Medicine, Department of Medicine, UCLA School of Medicine, 1980 – 1984.

o Acting Chief, Division of Clinical Immunology-Allergy, UCLA School of Medicine, 1977 - 1978

o Assistant Professor of Medicine, Department of Medicine, UCLA School of Medicine, 1977 – 1980

o Chief Scientific Officer and Founder, Tunitas Therapeutics, 2008 – 2016

o President and Founder, Sixal Incorporated, 2011 - present

PROFESSIONAL ACTIVITIES, UCLA:

Division of Clinical Immunology/Allergy Activities:

o Founder: Division of Clinical Immunology-Allergy, Department of Medicine, UCLA School of 

Medicine, 1977. The activity included 6 full-time faculty members and a broad array of research 

scientists, technicians, and administrative support persons. I have been funded continuously by 

the NIH since 1977 and currently have been awarded 2 NIH research grants

o Established the post-doctoral training program in Adult Clinical Immunology and Allergy. This was 

later combined with the ongoing Pediatric training program so that now I was Co-Director of the 

Conjoint Adult/Pediatric training program in Allergy and Clinical Immunology for about 25 

years. Initiated the UCLA Basic and Clinical Immunology conjoint teaching in 1977 that is now 

carried out in conjunction with the Department of Pediatrics. 

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Departmental Activities (selected):

o Department of Medicine Division Chiefs Committee, 1977 - 2006

o Department of Medicine Subspecialties Committee, 1999 - 2006

o Department of Medicine Honors Committee 1984 - 1987

o Department of Medicine Curriculum Committee 1989 - 1991

o Department of Medicine Chairman Search Committee 1991 - 1992

School of Medicine and Campus Activities (selected):

o Executive Board, UCLA Academic Senate, 1983 - 1984

o Interim Director - UCLA AIDS Center, 1985

o Associate Director - UCLA AIDS Center, 1986 - 1990

o Howard Hughes Faculty Search Committee, 1986 - 1991

o Dean's Bridge Grant Selection Committee 1995- 2010

o Co-Director, Center for Interdisciplinary Research in Immunologic Diseases Grant (CIRID) at 

UCLA, involving investigators from multiple School of Medicine Departments, as well as the 

School of Nursing, 1988 - to 1993.

o Director, UCLA Asthma, Allergy and Immunologic Disease Center 1993 – 2006, Co Director 2006 

- present. This Center, funded by the National Institutes of Health (National Institute of Allergy 

and Infectious Disease and the National Institute Environmental Health and Sciences) is 

dedicated to determining the relationship between environmental factors, the immune system and 

specific disease processes

o Principal Investigator: Basic and Clinical Immunology Training Grant, providing for graduate and 

post-graduate training positions to training preceptors in both the School of Medicine and the 

College of Letters and Science, 1990 - 2006

o Numerous search committees.

PROFESSIONAL ACTIVITIES, OUTSIDE UCLA:

National Scholarly Organization Activities (selected):

o American Academy of Allergy and Immunology, Basic and Clinical Immunology Section, ViceChair 1989 - 1990; Chair 1990 - 1991

o American Academy of Allergy and Immunology, Committees (active) Research Awards committee 

- Chair, Nominating committee, Primary Immunodeficiency Disease committee, Clinical and 

Diagnostic Immunology committee. 

o American Association of Immunologists, Program Committee - Clinical Immunology Section, CoChair 1994 - 1996

o American Association of Immunologists, Program Committee - Immediate Hypersensitivity Section, 

Co-Chair 1990 - 1991; Chair 1991 - 1993

o American Federation for Clinical Research, National Counselor, 1981 - 1986

o American Federation for Clinical Research, Public Policy Committee: 1982 - 1986

o American Federation for Clinical Research, Publications Committee: 1983 -1986

o Clinical Immunology Society, Council Member and Executive Committee. 1992- 2011

o Clinical Immunology Society, President, 1999 -2000

o Clinical Immunology Society, Publications Committee, 1987 - 1998, Chair, 1995 - 1998

o Dartmouth Medical School Admissions Support Committee, 1983 - 1988

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o National Institute of Allergy and Infectious Diseases: Co-chair for Allergy & Immediate 

Hypersensitivity 1996-7: Member 1989 - 1990

Task Force on Asthma and Other Allergic Diseases/New Initiatives in Immunology

o National Institute of Allergy and Infectious Diseases: Expert Panel on the Extramural Asthma and 

Allergy Research Program, Co-Chair, 2000

o Pan-American Group on Immunodeficiency, Co-founder and Member of Executive Council 1995 -

present

o National Institute of Allergy and Infectious Diseases: Expert Panel on Food Allergy Research, CoChair, 2003

o Task Force on Asthma and Other Allergic Diseases/New Initiatives in Immunology NIH, 2002

o U.S. Judiciary impartial expert witness: Swine Flu Litigation, 1984 - 1988

Research Peer Review Funding Responsibilities (selected):

o Immune Tolerance Network, Member and Co-Chair, Section on Allergy, Member of National 

Steering Committee and National Executive Committee, 2000 - 2014

o Advisory Council ad hoc member, National Institute of Allergy and Infectious Diseases, 1991

o Chair of Asthma, Allergy and Immunologic Disease Center Review, National Institute of Allergy 

and Infectious Diseases, 1994 and 1999.

o Co-chair of Human Immunology Think Tank, National Institute of Allergy & Infectious Diseases, 

2001

o Reviewer:

American Arthritis Foundation

Human Frontier Science Program Organization (Europe

Medical Research Council (Australia)

Medical Research Council (Canada)

Medical Research Council (United Kingdom)

National Science Foundation

NIH Study Sections: Ad Hoc: Immunobiology, Allergy and Immunology, Immunological 

Sciences, Experimental Immunology

Veterans’ Administration: Immunology Merit Review Board

Journal Stewardship:

o Editor-in-Chief: Clinical Immunology, 1999 – 2010,

o Special Editor/Editor emeritus, Clinical Immunology, 2011 - present

o Founder and Editor-in-Chief: AIDS Medical Update, 1983 - 1992

o Executive Editor: Clinical Immunology Spectrum, 1991 - 1996

o Associate Editor-in-Chief: The Immunologist, 1996 - 1999

o Associate Editor: AIDS Targeted Information Newsletter, 1987 - 1993

o Associate Editor: Journal of Immunology, 1982 - 1987

o Founder and Consulting Editor: AIDS Nursing Update, 1987 - 1992

o Associate Editor-in-Chief: Clinical Immunology & Immunopathology - 1998

o Editorial Board: 

Journal Allergy and Clinical Immunology, 1981 - 1986

Journal of Clinical Immunology, 1982 - 1989

Clinical Research, 1984 - 1986

Disease Markers, 1985 – 2012

o Member, Committee on Publishing Ethics, Elsevier 2008-2013

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TRAINING/TEACHING ACTIVITIES (selected):

o Co-Director: Combined Fellowship in Pediatric and Adult Immunology and Allergy, 1979 - 2003

o Director: Fellowship Program in Adult Clinical Immunology/Allergy (CIA), UCLA School of 

Medicine, 1977 - 1979

o American Academy of Allergy/Immunology: Trainee Award Committee Member, 1989 - 1991

o Member: Training Directors Committee, American Academy of Allergy and Immunology, 1980 -

2000

o Member: Training Directors Committee, American College of Allergy and Immunology, 1989 -

2000

o Chairman: UCLA Department of Medicine Honors Preceptor Program, 1984 - 1987

o Organizer and/or Instructor: various courses in Medicine and Microbiology & Immunology, as well 

as in continuing medical education, 1977 - present

PUBLIC SERVICE:

o Asthma and Allergy Foundation of America (Los Angeles Chapter): Board of Directors, 1981 -

1985

o Asthma and Allergy Foundation of America (Los Angeles Chapter): Medical Advisory Board, 1986 -

1999; Chairman, 1990 - 1999

o FDA Advisory Panel member - Allergenic products 1997 - 2002

o Immune Deficiency Foundation of America: Medical Advisory Board, 1990 - 2004

o PADI Foundation: Board of Directors, 1991- present, Secretary and Chief Financial Officer 1992 –

present.

o Chair, USC Children's Center Advisory Committee 1999-present

o Chair, Food Allergy Initiative Medical Advisory Board 2001 – 2006 

o External reviewer of the FDA research programs in the Laboratory of Immunobiochemistry, Division 

of Bacterial, Parasitic and Allergenic Products, Center for Biologics Evaluation and Research

PROFESSIONAL SOCIETIES:

o Association of American Physicians

o American Society for Clinical Investigation

o American Federation for Clinical Research

o American Association of Immunologists

o American Academy of Allergy and Clinical Immunology

o American College of Allergy and Immunology

o Clinical Immunology Society

o Collegium Internationale Allergologicum

o Los Angeles Society of Allergy and Clinical Immunology

o Pan-American Group on Immunodeficiency

o Society of Toxicology, Immunotoxicology Section

o Western Association of Physicians

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HONORS: (selected)

• Recipient: Allergic Diseases Academic Award; National Institute of Allergy and Infectious 

Diseases, 1978 – 1983.

• University Visiting Professorship: Singapore Post Graduate School of Medicine and Singapore 

General Hospital, Singapore, 1985.

• Swineford Memorial Lectureship: University of Virginia, Charlottesville, VA, 1987.

• Catholic University Visiting Lectureship in Immunology: Catholic University, Santiago, Chile, 1987

• Rabiner Visiting Professor: University of Oregon School of Medicine, Good Samaritan Hospital, 

Portland, OR, 1988.

• UCLA Visiting Professorship: Harbor General Hospital/UCLA, Torrance, CA, 1988.

• Robert Orange Memorial Lectureship, University of Toronto, Hospital for Sick Children, Toronto, 

Canada, 1988.

• Visiting Professor, National Jewish Center for Immunology, Denver, CO, 1990.

• American College of Allergy & Immunology Visiting Professor, University of Oklahoma, Tulsa, 

OK, 1991.

• American College of Allergy & Immunology Visiting Professor, Temple University, Philadelphia, 

PA., 1992.

• Goodman Family Visiting Professor, Santa Monica Hospital Medical Center, Los Angeles, CA 1994

• UCLA Medical Sciences Research Award Recipient, 1994.

• University of Illinois College of Medicine Visiting Professor 1995.

• Keynote speaker First Japanese Clinical Immunology and Allergy Society meeting and International 

Guest of Honor, Japanese Society of Immunology, Allergy and Otolaryngology, 1996.

• Arbesman Commemorative Lecturer - American Academy of Allergy, Asthma and Immunology, 

1997.

• National Institute of Allergy and Infectious Diseases 50th Anniversary Symposium Speaker, ATS, 

1999.

• Recipient, Stein Oppenheimer Award 1999.

• William Pierson Lectureship, American Academy of Allergy, Asthma and Immunology, Scripps 

Mercy Hospital, 2000.

• First Annual Feng Pao Hsii Lectureship, Singapore Society of Immunology, Rheumatology & 

Allergy Society, 2000.

• Keynote Speaker, Keystone Symposium on Asthma, Sante Fe, New Mexico, Feb. 2002

• Distinguished Visiting Professor in Immunology, Biology of Inflammation Center at Baylor College 

of Medicine, Feb. 2004.

• Presidential Award, Clinical Immunology Society, 2005.

• Physician-of-the-Year honoree, Asthma and Allergy Foundation of America, Los Angeles Chapter, 

2005.

• Carolyn and Warren Richards Allergy Lectureship, Children’s Hospital of Los Angeles, Keck School 

of Medicine, University of Southern California, 2006.

• Distinguished Service Award, Clinical Immunology Society, 2008

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PUBLICATIONS

Research Papers - peer reviewed

1. Saxon, A. and Higham, C.W.F. Identification and interpretation of growth rings in the secondary 

dental cementum of Ovis aris L. Nature. 219:634, 1968.

2. Saxon, A. and Higham, C.W.F. A new research method for economic prehistorians. American 

Antiquity. 34:303, 1969.

3. Ferm, V.H. and Saxon, A. Amniotic fluid volumes in experimentally induced renal agenesis and 

anencephaly. Experimentia. 27:1066, 1971.

4. Ferm, V.H., Saxon, A. and Smith, B.M. The teratogenic profile of sodium arsenate in the golden 

hamster. Arch Environ Health. 22:557, 1971.

5. Hoefnagel, D., Pomeroy, J., Wurster, D. and Saxon, A. Congenital athetosis, mental deficiency, 

dwarfism and laxity of skin and ligaments. Helv Paediat Acta. 26:397, 1971.

6. Saxon, A., Busch, G.J., Merrill, J.P. and Wilson, R. Renal transplantation in primary 

hyperoxaluria. Arch of Internal Med. 133:464, 1974.

7. Saxon, A. and Kattlove, H.E. Platelet inhibition by sodium nitroprusside, a smooth muscle 

inhibitor. Blood. 46:957, 1976.

8. Saxon, A., Feldhaus, J., and Robins, R.A. Single step separation of human T and B cells using 

AET treated SRBC rosettes. J Immunol Methods. 12:285, 1976.

9. Cline, M.J., Opelz, G., Saxon, A., Fahey, J.L. and Golde, D.W. Autoimmune panleukopenia. N 

Engl J Med. 295:1489, 1976.

10. O'Toole, C., Saxon, A. and Bohrer, R. Human lymph node lymphocytes fail to effect lysis of 

antibody coated target cells. Clin Exp Immunol. 27:165, 1977.

11. Bonavida, B., Robins, R.A. and Saxon, A. Lectin-dependent cellular cytotoxicity in man. 

Transplantation. 23:261, 1977.

12. Golde, D.W., Saxon, A. and Stevens, R.H. Macroglobulinemia and hairy-cell leukemia. N Engl 

J Med. 296:92, 1976.

13. Golde, D.W., Stevens, R.H., Quan, S.G. and Saxon, A. Immunoglobulin synthesis in hairy cell 

leukemia. Brit Journal Haematology. 35:359, 1977.

14. Saxon, A. and Portis, J. Lymphoid subpopulation changes in regional lymph nodes in squamous 

head and neck cancer. Cancer Res. 37:1154, 1977.

15. Saxon, A. and Portaro, J. Preservation of in vitro biologic functions in regional lymph node 

lymphocytes in squamous head and neck cancer. Cancer Res. 37:1159, 1977.

16. Saxon, A., Morledge, D. and Bonavida, G. Histamine receptor leukocytes (HRL): Organ and 

lymphoid subpopulation distributions in man. Clin Exp Immunol. 28:394, 1977.

17. Saxon, A., Stevens, R.H., Ashman, R.A. and Parker, N. Dual immune defects in nongranulomatous ulcerative jejunoileitis with hypogammaglobulinemia. Clin Immunol 

Immunopath. 8:272, 1977.

18. Saxon, A., Stevens, R.H. and Ashman, R.A. Regulation of immunoglobulin production in human 

peripheral blood leukocytes: Cellular interactions. J. Immunol. 118:1872, 1977.

19. Pratt, H.P.M., Fitzgerald, P.A. and Saxon, A. Synthesis of sterol and phospholipid induced by 

the interaction of phytohemagglutinin and other mitogens with human lymphocytes and their 

relation to blastogenesis and DNA synthesis. Cell Immunol. 32:160, 1977.

20. Saxon, A., Stevens, R.H., Raimer, S.J., Clements, P.J. and Yu, D.T.Y. Glucocorticoids 

administered in vivo inhibit human suppressor T lymphocyte function and diminish B 

lymphocyte responsiveness in in vitro immunoglobulin synthesis. J Clin Invest. 61:922, 1978.

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21. Saxon, A., Stevens, R.H., Quan, S.G. and Golde, D.W. Immunologic characterization of hairy 

cell leukemias in continuous culture. J Immunol. 120:777, 1978.

22. Fiala, M., Chatterjee, S.N., Carson, S., Poolsawat, S., Heiner, D.C., Saxon, A. and Guze, L.B. 

Cytomegalovirus retinitis secondary to chronic viremia in phagocytic leukocytes. Amer J 

Ophthalmol. 84:567, 1977.

23. Fiala, M. Chatterjee, S., Ellis, R., Imparato, B., Bahna, S. and Saxon, A. Fever of undetermined 

origin: Role of cytomegalovirus and Epstein-Barr virus. West J Med. 129:263-266, 1978.

24. Pratt, H.P.M., Saxon, A. and Graham, M.L. Membrane lipid changes associated with malignant 

transformation and normal maturation of human lymphocytes. Leukemia Research. 2:1, 1978.

25. Saxon, A. and Stevens, R.H. Suppression of immunoglobulin production in normal human 

blood characterization of the cells responsible and mediation by a soluble T lymphocyte derived 

factor. Clin Immunol Immunopath. 10:427, 1978.

26. Stevens, R.H., and Saxon, A. Anti-human helper T-lymphocyte antiserum: Generation and 

functional characterization. Clin Immunol Immunopath. 10:438, 1978.

27. Saxon, A., Stevens, R.H. and Golde, D.W. T-lymphocyte variant of hairy cell leukemia. Ann Int 

Med. 88:323, 1978.

28. Stevens, R.H. and Saxon, A. Immunoregulation in humans: Control of anti-tetanus toxoid 

antibody production after booster immunization. J Clin Invest. 62:1154, 1978.

29. Stevens, R.H., Thiele, C. and Saxon, A. The production of a soluble human T lymphocyte 

derived factor which substitutes for helper T lymphocytes in the in vitro production of 

immunoglobulin. Immunology. 36:407, 1979.

30. Saxon, A. and Stevens, R.H. Human T lymphocyte-derived helper factor (HHF): Cellular and 

physical characterization. Clin Immunol Immunopath. 12:82, 1979.

31. Fitchen, J.H., Cline, M.J., Saxon, A. and Golde, D.W. Serum inhibitors of hematopoiesis in a 

patient with aplastic anemia and systemic lupus erythematosus: Recovery after exchange 

plasmaphoresis. Amer J of Med. 66:537, 1979.

32. Saxon, A., Stevens, R.H. and Golde, D.W. Helper and suppressor T-lymphocyte leukemia in 

Ataxia Telangiectasia. N Engl J Med. 300:700, 1979.

33. Stevens, R.H. and Saxon, A. Reduced in vitro production of anti-tetanus toxoid antibody after 

repeated in vivo immunization with tetanus toxoid. J Immunol. 122:592, 1979.

34. Stevens, R.H. and Saxon, A. Differential synthesis of IgM and IgG antitetanus toxoid antibody 

in vitro following in vivo booster immunization of humans. Cell Immunol. 45:142, 1979.

35. Stevens, R.H., Macy, E., Morrow, C. and Saxon, A. Characterization of a circulating subpopulation of spontaneous anti-tetanus toxoid antibody producing B cells following in vivo

booster immunization. J Immunol. 122:2498, 1979.

36. Bluming, A., Cohen, H. and Saxon, A. Angioimmunoblastic lymphadenopathy with 

dysproteinemia: A pathogenetic link between physiologic lymphoid proliferation and malignant 

lymphoma. Amer J Med. 67:421, 1979.

37. Krantman, H.J., Stiehm, E.R., Stevens, R.H., Saxon, A. and Seeger, R.C. Abnormal B cell 

differentiation and variable increased T cell suppression in immunodeficiency with hyper-IgM. 

Clin Exp Immunol. 40:147, 1980.

38. Ashman, R.F., Saxon, A. and Stevens, R.H. Profile of multiple lymphocyte functional defects in 

acquired hypogammaglobulinemia derived from in vitro cell recombination analysis. J Allergy 

Clin Immunol. 65:242, 1980.

39. Saxon, A. and Stevens, R.H. Stimulation and regulation of human IgE production in vitro using 

peripheral blood lymphocytes. Clin Immunol Immunopath. 14:474, 1979.

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40. Saxon, A., Kobayashi, R.H., Stevens, R.H., Stiehm, E.R. and Siegel, S.C. In vitro analysis of 

humoral immunity with normal immunoglobulins in antibody deficiency. Clin Immunol 

Immunopath. 17:235, 1980.

41. Stevens, R.H., Tamaroff, M. and Saxon, A. Inability of patients with common variable 

hypogammaglobulinemia to generate lymphoblastoid B cells following booster immunization. 

Clin Immunol Immunopath. 16:336, 1980.

42. Saxon, A., Morrow, C. and Stevens, R.H. Subpopulations of circulating B cells and regulatory T 

cells involved in in vitro immunoglobulin E production in atopic patients with elevated serum 

immunoglobulin E. J Clin Invest. 65:1457, 1980.

43. Saxon, A., Tamaroff, M.A., Morrow, C. and Stevens, R.H. Impaired generation of spontaneous 

and mitogen-reactive anti-tetanus toxoid antibody producing B cells following repetitive in vivo 

booster immunization. Cell Immunol. 59:82, 1981.

44. Boxer, R.J., Sofen, H. and Saxon, A. The detection of transitional cell bladder cancer antigens 

on established cell lines. Invest Urology. 19:70, 1981.

45. Saxon, A., Kaplan, M. and Stevens, R.H. Isotype specific human B lymphocytes that produce 

immunoglobulin E in vitro when stimulated by pokeweed mitogen. J Allergy Clin Immunol.

66:231, 1980.

46. Stevens, R.H. and Saxon, A. Antigen-induced suppression of human in vitro pokeweed mitogen 

stimulated antibody production. Cell Immunol. 55:85, 1980.

47. Foon, K.A., Naiem, F., Saxon, A., Stevens, R.H. and Gale, R.P. Leukemia of T-helper 

lymphocytes: Clinical and functional features. Leukemia Research. 5:1, 1981.

48. Saxon, A., Thiele, C.J., Moroz, C. and Stevens, R.H. Adenosine receptor lymphocytes in 

humoral immunodeficiency. J Clin Immunol. 1:131, 1981.

49. Krantman, H.J., Saxon, A., Stevens, R.H. and Stiehm, E.R. Phenotypic heterogeneity in Xlinked infantile agammaglobulinemia with in vitro monocyte suppression of immunoglobulin 

synthesis. Clin Immunol Immunopath. 20:170, 1981.

50. Church, J.A., Isaccs, H., Saxon, A., Keens, T.G. and Richards, W. Lymphoid interstitial 

pneumonitis and hypogammaglobulinemia in children. Amer Rev Resp Dis. 124:491, 1981.

51. Cannon, R.A., Blum, P.M., Ament, M.E., Byrne, W.J., Soderberg-Warner, M., Seeger, R.C.,

Saxon, A. and Stiehm, E.R. Reversal of enterocolitis-associated combined immunodeficiency by 

plasma therapy. J Pediatrics. 101:711, 1982.

52. Saxon, A., McIntyre, R.E., Stevens, R.H. and Gale, R.P. Lymphocyte dysfunction in chronic 

graft versus host disease. Blood. 58:746, 1981.

53. Ahmed, R.A., Sofen, H. and Saxon, A. Detection of an antisquamous antibody in multiple 

kertoacanthoma. Clin Immunol Immunopath. 22:20, 1982.

54. Gottlieb, M.S., Schroff, R., Schanker, H.M., Weisman, J.D., Fan, P.T., Wolf, R.A. and Saxon, A. 

Pneumocystis carinii pneumonia and mucosal candidiasis in previously healthy homosexual men: 

Evidence of a new acquired cellular immunodeficiency. N Engl J Med. 305:1425, 1981.

55. Barbers, R.G., Shih, W.W.H. and Saxon, A. In vitro depression of human lymphocyte mitogen 

response (phytohemagglutinin) by asbestos fibres. Clin Exp Immunol. 48:602, 1982.

56. Schwartz, A.G., Targan, S.R., Saxon, A. and Weinstein, W.M. Sulfasalazine-induced 

exacerbation of ulcerative colitis. N Engl J Med. 306:409, 1982.

57. Ahmed, A.R., Stevens, R.H. and Saxon, A. Production of antibasement membrane zone 

antibody by peripheral blood leukocytes bullous pemphigoid patients. J Clin Immunol. 2:179, 

1982.

58. Thompson, L.F., Saxon, A., O'Connor, R.D. and Fox, R.I. Ectro-5'-nucleotidase activity in 

human T cell subsets: Decreased numbers of ecto-5'-nucleotidase positive cells from both 

OKT4+ and OKT8+ cells in patients with hypogammaglobulinemia. J Clin Invest. 71:892, 1983.

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59. Rohr, A., Hassner, A. and Saxon, A. Rhinopharynogoscopy for the evaluation of allergicimmunologic disorders. Ann Allergy. 50:380, 1983.

60. Ahmed, R.A., Murahata, R.I., Schroff, R.W., Stevens, R.H. and Saxon, A. Production of 

pemphigus antibody in vitro and analysis of T cell subsets. J Clin Immunol. 3:241, 1983.

61. Hassner, A. and Saxon, A. Inhibition of ongoing myeloma IgE synthesis in vitro by activated 

human T cells. J Immunol. 130:1567, 1983.

62. Schanker, H.M., Young, R., Cahan, L., Schroff, R. and Saxon, A. Effect of midbrain stimulus 

induced analgesia on immune function in humans. J Neuroimmunol. 5:185, 1983.

63. Denis, K.A., Wall, R. and Saxon, A. Human-human B cell hybridomas from in vitro stimulated 

lymphocytes patients with common variable immunodeficiency. J Immunol. 131:2273, 1983.

64. Hassner, A. and Saxon, A. Isotype-specific human suppressor T cells for IgE synthesis activated 

by IgE-Anti-IgE immune complexes. J Immunol. 132:2844, 1984.

65. Kodo, H., Gale, P. and Saxon, A. Antibody synthesis by bone marrow cells in vitro following 

primary and booster tetanus toxoid immunization in humans. J Clin Invest. 73:1377, 1984.

66. Rohr, A.S., Marshall, N.A. and Saxon, A. Successful immunotherapy for Triatoma protractainduced anaphylaxis. J All. Clin Immunol. 73:369, 1984.

67. Saxon, A., Hassner, A., Swabb, E.A., Wheeler, B. and Adkinson, N.F. Lack of cross-reactivity 

between Aztreonam, a monobactam antibiotic, and Penicillin in penicillin allergic subjects. J Inf 

Dis. 149:16, 1984.

68. Saxon, A. and Barnett, E. Human auto-anti-idiotypes regulating T cell mediated reactivity to 

tetanus toxoid. J Clin Invest. 73:342, 1984.

69. Ochs, H.D., Allred, R.U., Ammann, A.J., Budinger, M.D., Cowan, M.T., Fischer, S.H., Rousell, 

R.H., Saxon, A., Wara, D. and Wedgewood, R. Comparison of high dose, low dose intravenous 

immunoglobulin therapy in patients with primary immunodeficiency diseases. Amer J Med. 

76:78, 1984.

70. Kanowith-Klein, S. and Saxon, A. Fc epsilon receptors on human cell lines and peripheral blood 

lymphoctyes detected by binding of IgE immune complexes. J Clin Immunol. 5:38, 1985.

71. Saxon, A., Swabb, E. and Adkinson Jr., N.F. Investigation into the immunologic cross-reactivity 

of Aztreonam with other beta-lactam antibodies. Amer J Med. 78:19, 1985.

72. Schanker, H.M., Rajfer, J. and Saxon, A. Recurrent respiratory disease, azoospermia and nasal 

polyposis: A syndrome that mimics cystic fibrosis and immotile cilia syndrome. Arch Int Med.

145:2201, 1985.

73. Marshall, N., Liebhaber, M., Dyer, A. and Saxon, A. The prevalence of allergic sensitization to 

Triatoma protracta (Heteroptera: Reduviidae) in a Southern California U.S.A. Community. J 

Med Entomol. 23:117, 1986.

74. Kanowith-Klein, S. and Saxon, A. Regulation of ongoing IgE synthesis by human T cell 

supernatants derived from atopic and nonatopic donors. Int Arch Allergy Appl Immunol. 80:33, 

1986.

75. Ashida, E.R. and Saxon, A. Home intravenous immunoglobulin therapy by self-administration. 

J Clin Immunol. 6:306, 1986.

76. Marshall, M.S., Chapman, M.D. and Saxon, A. Species specific allergens from the salivary 

glands of Triatominae (Heteroptera: Reduviidae). J Allergy Clin Immunol. 78:430, 1986.

77. Chapman, M.D., Marshall, N.A. and Saxon, A. Identification and partial purification of species 

specific allergens from Triatoma protracta (Heteroptera: Reduviidae). J Allergy Clin Immunol. 

78:436, 1986.

78. Saxon, A., Mitsuyasu, R., Stevens, R., Champlin, R.E., Kimata, H. and Gale, R.P. Designed 

transfer of specific immune responses with bone marrow transplantation. J Clin Invest. 78:959, 

1986.

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79. Saxon, A., Tsui, F. and Martinez, O. Jacalin, an IgA binding lectin, inhibits differentiation of 

human B cells by both a direct effect and by activating T suppressor cells. Cell Immunol.

104:134, 1987.

80. Saxon, A. and Weinstein, R. Oral administration of bovine colostrum anti-cryptosporidia 

antibody fails to alter the course of human cryptosporidiosis. J Parasitology 73:413-415, 1987.

81. Sherr, E.H., Stein, L.D., Dosch, H.M. and Saxon, A. IgE enhancing activity directly and 

selectively affects activated B cells: Evidence for a human IgE differentiation factor. J Immunol. 

138:3836, 1987.

82. Kanowith-Klein, S., Saxon, A., Uittenbogaart, C.H. Constitutive production of B cell 

differentiation factor-like activity by human T and B cell lines. Euro. J. Immunol. 17:593-598, 

1987.

83. Kimata, H., Shanahan, F., Brogan, M., Targan, S. and Saxon, A. Modulation of ongoing human 

immunoglobulin synthesis by natural killer cells. Cell Immunol. 107:74, 1987.

84. Sherr, E.H., Saxon, A., Wells, J.R. Functional and phenotypic characterization of human B 

lymphocyte subsets isolated by unit gravity sedimentation. Int Arch Allergy Appl Immunol.

85:154, 1988.

85. Clement, L.T., Plaeger-Marshall, S., Hass, A., Saxon, A. and Martin, A.M. Bare lymphocyte 

syndrome: Consequences of absent class II major histocompatibility antigen expression for B 

lymphocyte differentiation and function. J Clin Invest. 81:669, 1988.

86. Saxon, A., Adelman, D. C., Patel, A., Hajdu, R. and Calandra, G.B. Imipenem cross-reactivity 

with penicillin in humans. J Allergy Clin Immunol. 82:213, 1988.

87. Sherr, E.H., Adelman, D.C., Saxon, A., Gilly, M., Wall, R. and Sidell, N. Retinoic acid Induces 

the differentiation of B cell hybridomas from patients with common variable immunodeficiency. 

J Exp Med. 168:55, 1988.

88. Kimata, H. and Saxon, A. A subset of natural killer cells is induced by immune complexes to 

display Fc receptors for IgE and IgA and demonstrate isotype regulatory function. J Clin Invest. 

82:160, 1988.

89. Kanowith-Klein, S., Hofman, F. and Saxon, A. Expression of Fc e receptors and surface and 

cytoplasmic IgE on human fetal and adult lymphopoietic tissue. Clin Immunol Immunopath. 

48:214, 1988.

90. Kimata, H., Sherr, E. and Saxon, A. Human natural killer cells produce a late acting B cell 

differentiation activity. J. Clin. Immunol. 8:381, 1988.

91. Macy, E., Kemeny, M. and Saxon, A. Enhanced ELISA: How to measure less than 10 

picograms of a specific protein (immunoglobulin) in less than 8 hours. FASEB Journal. 2:3003, 

1988.

92. Sherr, E., Macy, E., Kimata, H., Gilly, M. and Saxon, A. Binding the low affinity FceR on B 

cells suppresses ongoing human IgE synthesis. J. Immunol. 142:481, 1989.

93. Ch'ng, H.H., Shaw, D., Klesius, P. and Saxon, A. Inability of oral bovine transfer factor failed to 

eradicate cryptosporidial infection in a patient with congenital dysgammaglobulinemia. Clin 

Immunol Immunopath. 50:402, 1989.

94. Saxon, A., Giorgi, J.V., Sherr, E.H. and Kagan, J.M. Failure of B cells in common variable 

immunodeficiency to transit from proliferation to differentiation is associated with altered B cell 

surface molecule display. J Allergy Clin Immunol. 84:44, 1989.

95. Macy, E., Bulpitt, K., Champlin, R.E. and Saxon, A. Anaphylaxis to infusion of autologous 

bone marrow: An apparent IgE reaction to self, mediated by IgE antibody to bovine serum 

albumin. J. Allergy Clin Immunol. 83:871, 1989.

96. Kagan, J., Champlin R.E. and Saxon A. B-cell dysfunction following human bone marrow 

transplantation: Functional-phenotypic dissociation in the early post transplant period. Blood.

74:777, 1989.

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97. Ch'ng, H.H., Ganz, T. and Saxon, A. The utility of detecting autoantibodies against neutrophil 

cytoplasmic components in Wegener's granulomatosis. Ann Allergy. 63:411, 1989.

98. Kimata, H., Berenson, J., Kagan, J. and Saxon, A. Functional human T cell-B cell hybridomas 

established from fusion of normal T cells and an EBV transformed B cell line. Clin Immunol 

Immunopath. 54:134, 1990.

99. Saxon, A., Shanahan, F., Landers, C., Ganz, T. and Targan, S. A distinct subset of anti 

neutrophil cytoplasmic antibodies is associated with inflammatory bowel disease. J Allergy Clin 

Immunol. 86:202, 1990. 

100. Brieva, J.A., Martin, RA, Martinez-Maza, O, Kagan, J.M., Merrill, J, Saxon, A., Van Damme, 

J. and Stevens, R.H. Interleukin 6 is essential for antibody secretion by human in vivo antigeninduced lymphoblastoid B cells. Cellular Immunology 130:303, 1990.

101. Saxon, A, Ke, Z., Bahtee, L. and Stevens, RH. Soluble CD23 containing B cell supernatants 

induce IgE from peripheral blood B lymphocytes and co-stimulates with IL-4 in induction of 

IgE. J Allergy Clin Immunol. 86:333, 1990.

102. Adelman, D.C, Matsuda, T., Hirano, T., Kishimoto,T. and Saxon, A. Elevated serum 

interleukin-6 associated with a failure in B cell differentiation in common variable 

immunodeficiency. J Allergy Clin Immunol. 86:512, 1990.

103. Saxon, A. Macy, E, Witte, O., Tary-Lehmann, M., Denis, K. and Braun, J. Limited B cell 

repertoire in severe combined immunodeficient mice engrafted with peripheral blood 

mononuclear cells derived from immunodeficient or normal humans. J. Clin Invest. 87: 658, 

1991.

104. Zhang Ke, Z., Clark, E.A., and Saxon, A. CD40 stimulation provides an interferon-γ

independent IL-4 dependent IgE specific differentiation signal directly for human blood and 

tonsil B cells, J. Immunol., 146:1836-1842, 1991.

105. Sidell, N., Taga, T. Hirano, T., Kishimoto, T., and Saxon, A. Retinoic acid-induced growth 

inhibition of a human myeloma cell line via down-regulation of IL-6 receptors. J. Immunol.

146:3809-3814, 1991.

106. Braun, J., Galbraith, L., Valles-Ayoub, V., and Saxon, A. Human humoral immunodeficiency 

results from germinal center B cell arrest. Immun. Lett., 27:205-208, 1991.

107. Adelman, D.C., Yen, T.Y., Cumberland, W.G., Sidell, N. and Saxon A. 13-Cis retinoic acid 

enhances in vivo B-lymphocyte differentiation in patients with common variable 

immunodeficiency. J All. Clin Immunol. 88:705-712, 1991.

108. Saxon, A., Behle, K, Kurbe-Leamer, M., E. E. Max and Ke, Z. Inhibition of human IgE 

production via FceR-II stimulation results from a decrease in the mRNA for secreted but not 

membrane epsilon (e) heavy chains, J. Immunol., 147:4000-4006, 1991.

109. Tary-Lehmann, M. and Saxon, A. Human Mature T Cells which are Anergic in vivo Prevail in 

SCID Mice Reconstituted with Human Peripheral Blood (hu-PBL-SCID mice) J. Exp. Med.

175: 503-512, 1992.

110. Sogn, D., Evans, R., Shepard,G.M., Casale, T.B., Condemi, J.J., Greenberger, P.A., Kohler, 

P.F., Saxon, A., Summers, R.J., VanArsdel Jr, P.P., Massicot, J.G., Blackwelder, W.C. and 

Levine, B.B. Results of the NIAID collaborative clinical trial to test the predictive value of skin 

testing with major and minor penicillin derivatives in hospitalized adults. Arch. Int. Med. 

152:1025, 1992.

111. Zhang, K., Saxon, A., Max, E.E. Two unusual forms of human IgE encoded by alternative 

RNA splicing of ε heavy chain membrane exons. J. Exp. Med. 176:233-243, 1992.

112. Storek, J., Schmid, I., Ferrara, S., Saxon, A. A novel B-cell stimulation-proliferation assay 

using simultaneous flow cytometric detection of cell surface markers and DNA content. J. 

Immunol. Method. 151:261-267, 1992.

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113. Saxon, A., Sidell, N., Zhang, K. B-cells from subjects with CVI can be driven to Ig production 

in response to CD40 stimulation. Cell. Immunol., 144:169-181, 1992.

114. Storek, J., Ferrara, S., Rodriguez, C., and Saxon, A. Recovery of mononuclear cell subsets after 

bone marrow transplantation: Overabundance of CD4+ CD8+ dual-positive T cells reminiscent 

of ontogeny. J. Hematother. 1: 303-316, 1992.

115. Geha, R., Buckley, C.E., Greengberger, P., Patterson, R., Polmer, S., Saxon, A., Rohr, A., 

Yang, W., and Drouin, M. Aspartame is no more likely than placebo to cause 

urticaria/angioedema: Results of a multicenter, randomized, double-blind, placebo-controlled, 

crossover study. J. All. Clin. Immunol. 92:513-520. 1993.

116. Saxon, A., Keld, B., Braun, J., Dotson, A., and Sidell, N. Long Term Administration of 13-cis 

Retinoic Acid in Common Variable Immunodeficiency: Circulating IL-6 levels, B cell surface 

molecule display,and in vitro and in vivo B cell antibody production. Immunology, 80:477-487, 

1993.

117. Storek, J., Ferrara, S., Ku, N., Giorgi, J., Champlin, R.E., and Saxon, A. Reconstitution of Bcell immunity following bone marrow transplantation: Recapitulation of Ontogeny? Bone 

Marrow Transplantation. 12:387-398, 1993.

118. Zhang, K., Max, E.E., Cheah, H-K., and Saxon, A. Complex alternative RNA splicing of 

ε immunoglobulin transcripts produces mRNAs encoding four potential secreted protein 

isoforms. J. Biol. Chem. 269: 456-462, 1994.

119. Uittenbogaart, C.H., Anisman, D.J., Tary-Lehmann, M., Vollger, L.W., Breit, T.M., Van 

Dongen, J.J.M., and Saxon, A. The SCID mouse environment causes immunophenotypic 

changes of human immature T cell lines. Int. J. Cancer. 56: 546-551, 1994.

120. Zhang, K., Mills, F.C., Saxon, A. Switch Circles from IL-4 Directed e Class Switching from 

Human B Lymphocytes: Evidence for Direct, Sequential and Multiple Step Sequential Switch 

from Mu to Epsilon Immunoglobulin Heavy Chain Gene. J. Immunol., 152: 3427-3435, 1994.

121. Diaz-Sanchez, D., Chegini, S., Zhang, K, Saxon, A. CD58 (LFA-3) Stimulation Provides a 

Signal for Human Isotype switching and IgE Production Distinct from CD40. J. Immunol. 

153:10-20, 1994. 

122. Diaz-Sanchez, D., Dotson, A.R., Takenaka, H., Saxon, A., Diesel exhaust particles induce local 

IgE production in vivo in humans and alter the pattern of IgE mRNA isoforms. J. Clin. Invest.

94:1417-25, 1994.

123. Tary-Lehmann, M., Lehmann, P.V., Schols, D., Grazia-Roncarolo, M., Saxon, A. Anti-SCID 

mouse reactivity shapes the human CD4+ repertoire in hu-PBL-SCID chimeras. J. Exp. Med. 

180:1817-1827, 1994.

124. Storek, J., King, L., Ferrara, S., Marcello, D., Saxon, A., Braun, J. Abundance of a restricted 

fetal B cell repertoire in marrow transplant recipients. Bone Marrow Trans., 14: 783-790, 1994.

125. Storek, J., Ferrara, S., Hultin, L.E., Ku, N., Giorgi, J.V., Champlin, R.E., and Saxon, A. B cell 

dysfunction after bone marrow transplantation is associated with decreased Ca++ flux upon 

membrane Ig crosslinking. Clin. Immunol Immunopath. 72:210-6, 1995.

126. Takenaka, H., Zhang, K., Diaz-Sanchez, D., Tsien, A., Saxon, A., Enhanced human IgE results 

from exposure to the aromatic hydrocarbons in diesel exhaust: direct effects on B cell IgE 

production, J. All. Clin. Immunol, 95:103-115, 1995.

127. Zhang, K., Cheah, H-K., Saxon, A., Secondary deletional recombination of rearranged switch 

region in Ig isotype switched B cells: A mechanism for isotype stabilization. J. Immunol. 154: 

2237-2247, 1995.

128. Zhang, K, Diaz-Sanchez, D., Saxon, A. Germ-line human epsilon heavy chain gene RNA 

transcripts utilize the full range of alternative 3' splicing seen in productive epsilon mRNAs, 

Immunology, 85: 228-235, 1995.

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129. Xu F., Saxon, A, Nguyen, A., Zhang, K., Diaz-Sanchez, D., Nel, A. IL-4 activates a Stat protein 

which interacts with a GAS-like sequence upstream of the Iε exon in a human B-cell line: 

Evidence for the involvement of JAK3 kinase and IL-4-Stat., J. Clin. Invest., 96:907-914, 1995.

130. Diaz-Sanchez, D., Zhang, K., Nutman, T.B., Saxon, A., Differential regulation of alternative 3' 

splicing of human epsilon mRNA variants. J. Immunol, 155: 1930-1941, 1995.

131. Tary-Lehmann, M., Saxon, A., Lehmann, P.V. The human immune system in hu-pbl-SCID 

mice. Immunology Today. 16:529-33 1995.

132. Saxon, A, Keld, B., Diaz-Sanchez, D., Guo, B-C., Sidell, N. B cells from a distinct subset of 

patients with common variable immunodeficiency have increased CD95 (Apo-1/fas) and 

diminished CD38 expression and undergo enhanced apoptosis: rescue by CD40 and IL-4, Clin 

Exp. Immunol., 102: 17-25, 1995.

133. Fujieda, S., Zhang, K, Saxon, A. IL-4 plus CD40 mAb Induces Human B Cell Gamma 

Subclass Specific Isotype Switch: Switching to g1, g3 and g4 but not g2. J. Immunol., 155: 

2318-2328, 1995.

134. Guo, B. C. and Saxon, A. B Cell Lines from a Subset of Patients with Common Variable 

Immunodeficiency Undergo Enhanced Apoptosis Associated with Increased CD95 (Apo-1/fas) 

Display, Diminished CD38 Expression, and Decreased IgG and IgA Production, Cell 

Immunology, 166:83-92, 1995.

135. Lyczak, J., Zhang, K., Saxon, A., Morrison, S., Expression of Novel Secreted Isoforms of 

Human Immunoglobulin E Proteins. J. Biol. Chemistry, 271:3428-36, 1996.

136. Diaz-Sanchez, D., Tsien, A., Casillas, A., Dotson, A.R., Saxon, A. Enhanced Nasal Cytokine 

Production in Human Beings after in vivo Challenge with Diesel Exhaust Particles. J. Allergy. 

Clin. Imunol., 98:114-23, 1996.

137. Fujieda,S., Waschek, J.A., Zhang, K, Saxon, A. Vasoactive intestinal peptide induces Sa/Sm 

switch circular DNA in human B cells, J. Clin. Invest. 98:1527-32, 1996.

138. Fujieda, S., Lin, Y.Q., Saxon, A, and Zhang, K. Multiple Types of Chimeric Germ-line Ig 

Heavy Chain Transcripts in Human B Cells: Evidence for trans-splicing of Immunoglobulin 

RNA. J. Immunol., 157: 3450-9, 1996

139. Peterson, B, and Saxon A., Global Increases in Allergic Respiratory Disease: The Possible Role 

of Diesel Exhaust. Ann. All. Asthma, Immunol, 77:263-8, 1996.

140. Fujieda, S., Saxon, A., Zhang, K., Direct Evidence that g1 and g3 switching in human B cells is 

interleukin-10 dependent., Molecular Immunology, 1335-43, 1997.

141. Tsien, A., Diaz-Sanchez, D., Saxon, A. The Organic Component of Diesel Exhaust Particles 

and Phenanthrene, a Major Polyaromatic Hydrocarbon Constituent, Enhance IgE Production by 

IgE- secreting EBV-transformed Human B cells in vitro, Toxicology and Applied 

Pharmacology, 142:256-63, 1997.

142. Saxon, A, Diaz-Sanchez, D., Zhang, K. Regulating expression of distinct human secreted IgE 

proteins produced by alternative RNA splicing, Biochemical Society Transactions 25:383-387, 

1997.

143. Diaz-Sanchez, D., Tsien, A, Fleming, J., Saxon, A. Combined Diesel Exhaust Particulate and 

Ragweed Allergen Challenge Markedly Enhances In Vivo Nasal Ragweed-Specific IgE and 

Skews Cytokine Production to a TH2-Type Pattern, J. Immunol, 158:2406-2413, 1997.

144. Thompson, AA, Talley, JA, Do, HN, Kagan, HL, Kunkel, L, Berenson, J. Cooper, M., Saxon, 

A, Wall, R. Aberrations in the B cell receptor B29 (CD79b) gene in chronic lymphocytic 

leukemia. Blood, 90:1387-94, 1997.

145. Ng, D, Kokot, N, Faris, M, Saxon, A, Nel, A. Macrophage activation by polycyclic aromatic 

hydrocarbons: Evidence for the involvement of stress-activation protein kinases, AP-1 and antioxidant response elements. J. Immunol, 161:942-951, 1998

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146. Fujieda, S, Sieling, P.A., Modlin, R.L., Saxon, A. CD1b-restricted T cells influence IgG 

subclass and IgE production, J. Allergy Clin. Immunol. 101:545-51, 1998.

147. Wakim, M, Alazard, M, Yajima, A, Speights, D, Saxon, A, Steihm, ER. High dose intravenous 

immunoglobulin in atopic dermatitis and hyper-IgE syndrome. Ann. Allergy, Asthma, Immunol. 

83: 53-58, 1998.

148. Fujieda, S. Diaz-Sanchez, D., Saxon, A. Combined Nasal Challenge with Diesel Exhaust 

Particles and Allergen Induces In Vivo IgE Isotype Switching, Am. J. Respir. Cell Mol. Biol. 19: 

507-512, 1998

149. Nel, AE, Diaz-Sanchez, D, Ng, D, Hiura, T, Saxon, A. Enhancement of allergic inflammation 

by the interaction between diesel exhaust particles and the immune system. J. Allergy Clin. 

Immunol., 102:539-554, 1998.

150. Wang, M., Saxon, A., Diaz-Sanchez, D. Early IL-4 production driving Th2 differentiation in a 

human in vivo model is mast cell derived. Clinical Immunology, 90:47-54, 1999.

151. Thompson, AA, Do, HN, Saxon, A, Wall, R. Widespread B29 (CD79b) gene defects and loss 

of expression in chronic lymphocytic leukemia. Leukemia and Lymphoma, 35:561-9, 1999.

152. Diaz-Sanchez, D, Tsien, A, Flemming, J, Saxon, A. Effect of topical fluticasone propionate on 

the mucosal allergic response induced by ragweed allergen and diesel exhaust particle challenge. 

Clinical Immunology 90:313-320, 1999.

153. Saxon, A., Nel, A.E., Diaz-Sanchez, D. Diesel particulates in allergic airway disease. Jap. J. 

Rhinology 38:123-8, 1999.

154. Diaz-Sanchez, D, Wang, M, Penichet-Garcia, M, Jyrala, M,. Saxon, A, Nasal challenge with 

diesel exhaust can induce sensitization to a neoallergen in the human mucosa. J. Allergy Clin. 

Imm. 104:1183-8, 1999.

155. Saxon, A., Ownby, D., Huard, T., Parsad, R., Roth H.D. Prevalence of IgE to Natural Rubber 

Latex in unselected blood donors and performance characteristics of Alastat® testing, Annals of 

Allergy, Asthma and Immunology, 84:199-206, 2000.

156. Geha, RS, Beiser, A, Ren, C, Patterson, R, Greenberger, PA, Grammer, LC, Ditto, AM, Harris, 

KE, Shaughnessy, MA, Yarnold, PR, Corren, J, Saxon, A. Multicenter, double-blind placebo 

controlled multiple challenge evaluation of reported reactions to monosodium glutamate J. 

Allergy Clin Imm., 106:973-980, 2000.

157. Diaz-Sanchez, D, Jyrala, M, Ng, D, Nel, A.E., Saxon, A In vivo challenge with diesel exhaust 

particles enhances expression of the C-C chemokines Rantes, MIP-1a and MCP-3 in humans. 

Clinical Immunology, 97: 140-5, 2000

158. Diaz-Sanchez D, Penichet-Garcia M, Saxon A. Diesel exhaust particles directly induce 

activated mast cells to degranulate and increase histamine levels and symptom severity. J 

Allergy Clin Immunol. 2000 Dec;106(6):1140-6.

159. Chan, L, Lyczak, JB, Zhang, K, Morrison, S, Saxon, A. The novel human IgE epsilon heavy 

chain, epsilon tailpiece, is present in plasma as part of a covalent complex. Molecular 

Immunology, 37:241-52, 2001

160. Heo, Y., Saxon, A. , and Hankinson, O, Effect of diesel exhaust particles and their components 

on the allergen-specific IgE and IgG1 response in mice,

. Toxicology, 159: 143-158, 2001.

161. Diaz-Sanchez, Penichet-Garcia, M, Saxon, A. Differential effects diesel exhaust particle 

chemicals vs the carbon core human allergic responses, Immunology 107: 55-61, 2002

162. Zhang, K., Zhang, L,. Yamada, T, Vu M.V., Lee, A, Saxon A., Efficiency of Iε promoterdirected switch recombination in GFP expression based switch constructs works synergistically 

with other promoter and/or enhancer elements but is not tightly linked to the strength of the 

transcriptional activity. European J. Immunol. 32:424-34, 2002

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163. Zhu, DC, Kepley, CL, Zhang, M, Zhang, K, Saxon, A. A Novel Human Ig Fcγ-Fcε Bifunctional 

Fusion Protein Inhibits FcεRI-Mediated Degranulation, Nature Medicine 8:518-22, 2002.

164. Devouassoux, G., Saxon, A., D.D. Metcalfe D.D., Prussin, C, Colomb, M.G., Brambilla, C., 

Diaz-Sanchez, D., Chemical Constituents of Diesel Exhaust Particles Induce IL-4 Production by 

Human Basophils, J. All. Clin. Imm., 109:847-853, 2002.

165. Yamada T, Zhu D, Saxon A, Zhang K. CD45 controls interleukin-4-mediated IgE class switch 

recombination in human B cells through its function as a Janus kinase phosphatase. J Biol 

Chem. 2002 Aug 9;277(32):28830-5

166. Zhang K, Zhang L, Zhu D, Bae D, Nel A, Saxon A. CD40-mediated p38 mitogen-activated 

protein kinase activation is required for immunoglobulin class switch recombination to IgE. J 

Allergy Clin Immunol. 2002 Sep;110(3):421-8.

167. Zhou, C, Saxon, A and Zhang K., Human Activation-Induced Cytidine Deaminase is induced 

by IL-4 and negatively regulated by CD45: Implication for CD45 as a Janus Kinase 

Phosphatase in Antibody Diversification, J. Immunol., 170, 1887-1893, 2003.

168. Kepley, CL, Zhang, K, Zhu, DC, Saxon, A: FcεRI-FcγRII Co-Aggregation Inhibits IL-16 

Production From Human Langerhans-Like Dendritic Cells, Clin Imm. 108(2):89-94, 2003.

169. Yamada, T, Zhu, DC, Zhang, K. Saxon, A, Inhibition of IL-4-induced class switch 

recombination by a human Ig Fc gamma -Fc epsilon chimeric protein, J. Biol. Chem. 

278:32818-32824, 2003.

170. Gilliland, FD, Li YF, Saxon, A, Diaz-Sanchez, D. Glutathione-S-Transferase M1 and P1 

Genotypes Protect Against Xenobiotic Enhancement of Allergic Responses. Lancet, 363:119-

125, 2004.

171. Bastain, TM, hFrank D. Gilliland, FD, Li, YF., Saxon, A, Diaz-Sanchez, D. Intra-Individual 

Reproducibility of Nasal Allergic Responses to Diesel Exhaust Particles Indicates a Susceptible 

Phenotype. Clin. Immun. 109:130-6, 2004.

172. Kepley, CL, Taghavi, S, Mackay, G, Zhu, D, Morel, PA Zhang, K, Ryan, JJ, Satin, LS, Zhang, 

M, Pandolfi, PP and Saxon, A. Co-Aggregation of FcγRII With FcεRI on Human Mast Cells 

Inhibits Antigen-Induced Secretion and Involves SHIP-Grb2-Dok Complexes, J. Biol. Chem,

279:35139-49, 2004.

173. Corren J, Diaz-Sanchez D, Saxon A, Deniz Y, Reimann J, Sinclair D, Davancaze T, Adelman 

D. Effects of omalizumab, a humanized monoclonal anti-IgE antibody, on nasal reactivity to 

allergen and local IgE synthesis. Ann Allergy Asthma Immunol. 93:243-8, 2004.

174. Zhang, K, Kepley, CL, Terada, T, Daocheng Zhu, DC, PhD, Perez, H, Saxon, A. Inhibition of 

Allergen Specific IgE Reactivity by a Human Ig Fcγ-Fcε Bifunctional Fusion Protein, J Allergy 

Clin Immunol. 114:321-7, 2004.

175. Zhu, D, Kepley, CL, Zhang, K, Terada, T, Yamada, T, Saxon, A. A Chimeric Human –Cat 

Fusion Protein Blocks Cat-induced Allergy, Nature Medicine, Nature Medicine. 11:446-9, 2005.

176. Yamada, T, Zhang, K, Yamada, A, Daocheng Zhu, D, Saxon A., Lymphocyte Stimulator 

activates p38 MAPK in Human Ig Class Switch Recombination, Amer. J. Resp. Cell Mol. Biol,

32: 388-94, 2005.

177. Riedl, MA, Landaw, EM, Saxon A, Diaz-Sanchez, D. Initial High-dose Nasal Allergen 

Exposure Prevents Allergic Sensitization to a Neoantigen. J Immunol, 174:7440-5, 2005

178. Terada, T, Zhang, K, Belperio, J, Londhe, V, Saxon A., A chimeric human-cat Fcγ-Fel d1 

fusion protein inhibits systemic, pulmonary and cutaneous allergic reactivity to intratracheal 

challenge in mice sensitized to Fel d1, the major cat allergen, Clinical Immunology, 120:45-56, 

2006.

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179. Saxon A, Zhu D, Zhang K, Chan LA, Kepley CL. Recent advances in the use of genetically 

engineered negative signaling molecules to treat allergic diseases. Arb Paul Ehrlich Inst. 

Bundesamt Sera Impfstoffe Frankf AM. 2006;(95):223-31

180. St. Clair, W.E. Larry A. Turka, L.A., Saxon, A., Jeffrey B. Matthews,JB,. Sayegh, MH, 

Eisenbarth, GS, Bluestone, J., New Reagents on the Horizon for Immune Tolerance, Annual 

Review of Medicine, 2007. 58:329-46

181. Zhang K, Zhu D, Kepley C, Terada T, Saxon A. Chimeric human fcgamma-allergen fusion 

proteins in the prevention of allergy. Immunol Allergy Clin North Am. 27:93-103, 2007.

182. Allen L, Kepley C, Saxon A, Zhang K. Modifications to a Fcγ-Fcε fusion protein alter its 

effectiveness in the inhibition of FcεRI-mediated functions. J. Allergy Clin. Immunol;120:462-

8, 2007

183. Mertsching, E, Bafetti, L, Hess, H, Stuart Perper, S, Giza, K Allen, L, Negrou, E, Hathaway, K, 

Hopp, J, Chung, J. Daniel Perret, D, Michael Shields, M, Saxon, A and. Kehry, MR, A mouse 

FcγFcε protein that inhibits mast cells through activation of FcγRIIB, SH2 domain-containing 

inositol phosphatase 1, and SH2 domain-containing protein tyrosine phosphatases . J. Allergy 

Clin. Immunol, 121: 441-447, 2008

184. Saxon, A, Kepley, C, Zhang, K. “Accentuate the negative, eliminate the positive”: Engineering 

allergy therapeutics to block allergic reactivity via negative signaling. J. Allergy Clin. Immunol, 

121: 320-5, 2008. 

185. Riedl, MA, Saxon, A, Diaz-Sanchez, D. Oral Sulforaphane increases Phase II antioxidant 

enzymes in the human upper airway. Clin Immunol, 130:244-51, 2009.

186. Behnecke, B., Wei L., Chen L., Saxon, A., Zhang, K. A Chε-Based Allergen Gene Vaccine 

Platform That Targets Human Antigen Presenting Cells via the High Affinity IgE Receptor 

(FcεRI), J. Allergy Clinical Immunology;124:108-13, 2009.

187. Lin E., Saxon A, Riedl M., Penicillin Allergy: Value of Including Amoxicillin as a Determinant 

in Penicillin Skin Testing, Int. Arch All Imm. 2010;152: 313-318, 2010, PMID: 20185923

188. Li W, Zhang Z, Saxon A, Zhang K. Prevention of oral food allergy sensitization via skin 

application of food allergen in a mouse model. Allergy. 2012 doi: 10.1111/j.1398-9995.2012. 

PubMed PMID: 22339388.

189. Zhang, K, Liu J, Truong T, Zukin E, Chen W, Saxon A, Blocking allergic reaction through 

targeting surface-bound IgE with low affinity anti-IgE antibodies, J. Immunol Blocking Allergic 

Reaction through Targeting Surface-Bound IgE with Low-Affinity Anti-IgE Antibodies. J. 

Immunol. 2017;198(10):3823-3834. doi: 10.4049/jimmunol.1602022. PubMed PMID: 

28396318.

Research Papers - non-peer reviewed

190. Gale, R.P., Opelz, G., Mickey, M.R., Graze, P.R. and Saxon, A. Immunodeficiency following 

allogeneic bone marrow transplantation. Transplant Proc. 10:223, 1978.

191. Opelz, G., Gale, R.P., Feig, S.A., Walker, J., Terasaki, P.I. and Saxon, A. Significance of HLA 

and non-HLA antigens in bone marrow transplantation. Transplant Proc. 10:43, 1978.

192. Saxon, A. and Stevens, R.H. Synthesis of human IgE in vitro in normals and high IgE atopy. Int 

Archs Allergy Appl Immunol. 66:55, 1981.

193. Saxon, A., Mawhinney, H. and Stevens, R.H. Alterations in functional human B cell subsets that 

produce IgG and IgE in vitro by repeated antigen exposure in vivo. In: Human B cell function: 

activation and regulation. A.S. Fauci and R.P. Baillieux, eds. Raven Press. 1982, p.73.

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194. Denis, K.A., Wall, R. and Saxon, A. Human-human hybridomas in the study of 

immunodeficiencies. In: Human hybridomas and monoclonal antibodies. Engleman, Foung, 

Larrack and Raubitschek, eds., Plenum Pub. Co., New York. 1985, p. 293.

195. Kimata, H. and Saxon, A. Natural killer cell interaction with IgE in the control of ongoing 

human IgE synthesis. Int Arch Appl Immmunol. 82:419, 1987.

196. Sherr, E. and Saxon, A. Fc epsilon receptor mediated suppression: A mechanism for the 

suppression of ongoing IgE synthesis. Int Arch Appl Immunol. 82:414, 1987.

197. Saxon, A. and Kimata, H. Human Natural Killer cells and their Fc epsilon receptors in the 

regulation of IgE and other immunoglobulin isotypes. In: Advances in the Biosciences (Allergy 

and Molecular Biology), El Shami, A.S. and Merrett, T. G. (eds.), 74:359, 1989.

198. Stevens, R.H., Brieva,J.A., Martin, R.A. and Saxon, A. Regulation of specific antibody 

production via CD23. In: Monographs in Allergy, Gordon, J., (ed.), Switzerland, p. 169-177. 

1991.

199. Saxon, A., Zhang, K., Max, E.E. Regulation of human B cell production of IgE proteins. Proc 

9th Sandoz Immunopharmacology Symposium, 1991.

200. Braun, J., Saxon, A., Wall, R., and Morrison, S.L. The second century of the antibody: 

Molecular perspectives in regulation, pathophysiology, and therapeutic applications. Western J. 

Med., 157:158-168, 1992.

201. Saxon, A., Zhang, K., and Max, E.E. Human ε mRNAs using membrane sequence encode for 

two membrane forms of IgE and a novel second secreted IgE. In: Transactions of the 

Association of American Physicians. Baltimore, MD. 93-99, 1992.

202. Storek, J. and Saxon, A. Reconstitution of B-cell immunity following bone marrow 

transplantation. Bone Marrow Transplant. 9:395-408, 1992.

203. Saxon, A, Max, EE, Diaz-Sanchez, D, Zhang, K. Alternative RNA Splicing of Epsilon 

Transcripts Produces mRNAs Encoding Two Membrane and Four Secreted IgE Isoforms. Int. 

Arch. All. Immunol., 107: 45-47, 1995.

204. Diaz-Sanchez, D, Saxon, A, The Effect of Diesel Exhaust Particles on Allergic Disease, Allergy 

& Clinical Immunology International 8:57-61, 1996.

205. Geha RS; Beiser A; Ren C; Patterson R; Greenberger PA; Grammer LC; Ditto AM; Harris KE; 

Shaughnessy MA; Yarnold PR; Saxon A, et al. Review of alleged reaction to monosodium 

glutamate and outcome of a multicenter double-blind placebo-controlled study. Journal of 

Nutrition, 2000 Apr, 130(4S Suppl):1058S-62S.

206. Saxon, A. and Diaz-Sanchez, D. Diesel Exhaust as a Model Xenobiotic in Allergic 

Inflammation. Immunopharmacology, 48: 325-9, 2000.

207. Zhang, K., Behnecke, A., Saxon, A and Li W. An IgE-based Polyplex Allergen Gene Vaccine 

That Targets Dendritic Cells; A Novel Therapeutic Approach for Severe Food Allergy, 

Proceeding of the 27th CIA Symposium (van Ree, Ring & Marone Editors), 2010, pg 261-265.

Reviews and Book Chapters

208. Saxon, A. Dendrochronology. Science in Archaeology. 7:4, 1967.

209. Saxon, A. Immediate hypersensitivity: Approach to diagnosis. In Manual of Allergy and 

Clinical Immunology. Fisher, T.J., Lawlor, G. (eds.), Little Brown Co. Boston. 1981, p. 15.

210. Saxon, A. Assessment of T-cell help and suppression of B-cell function. In: Manual of Clinical 

Immunology. Rose, N.R. and Friedman, H. (eds.), Amer Soc Micro. Washington, D.C. 1980, p. 

151.

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211. Wall, R. and Saxon, A. Molecular approaches to human immune functions and disorders. In: 

Genetic Disease: Diagnosis and Treatment. Dietz, A.A. (ed.). Amer Assoc Clin Chem. 

Washington, D.C. 1983, p. 131.

212. Saxon, A. Immediate hypersensitivity reactions to beta-lactam antibiotics. Rev of Inf Dis. 

5:5368, 1983.

213. Saxon, A. Insect allergy. In: Allergy and Clinical Immunology. Beall, G. (ed.). John Wiley and 

Sons Inc, New York City. 1983, p. 201.

214. Thompson, L.F., Saxon, A., O'Connor, R. and Fox, R. Ecto-5'- nucleotidase as a cell surface 

marker of human T lymphocyte subpopulations. In: Intercellular Communication in Leukocyte 

Function. Parker, J.W. and O'Brien, R.L. (eds.). Wiley and Sons, New York City. 1983, p. 189.

215. Adkinson, N.F., Saxon, A., Spence, M.R. and Swabb, E.A. Cross-allergenicity and 

immunogenicity of aztreonam. Rev Inf Disease. 7:613, 1983.

216. Saxon, A. Reconstitution of specific immunity following bone marrow transplantation. UCLA 

Symposium on Molecular and Cellular Biology. Gale, R.P. and Chaplin, R. (eds.). Alan R. Liss, 

Inc. Progress in Bone Marrow Transplantation. 53:623-633, 1987.

217. Saxon, A. and Stiehm, R. The B cell system. In: Immunologic Disorders in Infants and 

Children. Stiehm, E.R. (ed). W.B. Sanders Co. 1988.

218. Saxon, A. Immediate hypersensitivity: Approach to diagnosis. In: Manual of Allergy and 

Clinical Immunology. Fisher, T.J. and Lawlor, G. (eds.). Little Brown Co. Boston, 2nd Edition. 

1987.

219. Saxon, A., Beall, G., Rohr, A. and Adelman, D. Immediate hypersensitivity reactions to betalactam antibiotics. Annals of Int Med. 107:204, 1987.

220. Adelman, D.C. and Saxon, A. Recurrent bacterial infections and cellulitis in a 29 year old 

woman with a history of hypogammaglobulinemia. Ann Allergy. 59:403, 1987.

221. Saxon, A. Antibiotic choices in the penicillin allergic patient. Postgraduate Medicine. 83:135, 

1988.

222. Saxon, A. and Kaplan A. Immediate hypersensitivity. Immunology and Allergy Clinics of 

North America. 8:145, 1988.

223. Saxon, A. and Campen, V. AIDS: State of the art, spring 1988. J Allergy Clin Immunol. 

81:796, 1988.

224. Saxon, A. Aztreonam in the management of gram-negative infections in penicillin allergic 

patients: A review. Ped Infec Dis.J. 8: 124, 1989.

225. Storek, J and Saxon, A. Reconstitution of B-cell immunity following bone marrow 

transplantation. Bone Marrow Transplant. 1992, 9:395-408.

226. Saxon, A. Immunodeficiency: Functional B-cell Studies. In: Manual of Clinical Laboratory 

Immunology. Rose, N.R., Friedman, H. and Fahey, J.L..(eds.). Amer Soc Micro. Washington, 

D.C. 1992, p 403-8.

227. Adelman, D and Saxon, A. Immediate hypersensitivity: Approach to diagnosis. In: Manual of 

Allergy and Clinical Immunology. Lawlor, G. and Adelman, D. (eds.). Little Brown Co. Boston, 

3rd Edition. 1994. p 18-39.

228. Saxon, A., Diaz-Sanchez, D., Zhang, K., The Allergic Response in Host Defense. In Clinical 

Immunology, R.R. Rich, T.A. Fleisher, B.D. Schwartz, W.T. Shearer, and W. Strober, (eds.) 

Mosby Co. St. Louis, MO., p 847-62, 1996.

229. Zhang, K. and Saxon, A., Human IgE: Production of a family of IgE proteins by alternative 

splicing of the 3' end e RNA. in Molecular Mechanisms of IgE Regulation, Vercelli, D. (ed), 

Wiley & Sons, London, p191-205-224, 1997

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230. Zhang, K. and Saxon, A., Human IgE: Isotype switching from μ to ε Ig heavy chain gene in 

human B cells as determined by switch circle analysis. in Molecular Mechanisms of IgE 

Regulation, Vercelli, D. (ed), Wiley & Sons, London,191-204, 1997

231. Hardin, BD, Kelman, BJ, Saxon, A. Adverse human health effects associated with molds in the 

indoor environment. J Occup Environ Med 2003 May;45(5):470-8.

232. Saxon, A. What impact will the Immune Tolerance Network have on the future treatment of 

allergic diseases? Clin Exp Allergy, 34:1657-9, 2004.

233. Saxon, A., Zhu, D, Zhang, K. Allen, L.C., Kepley, C.L, Genetically engineered negative 

signaling molecules in the immunomodulation of allergic diseases, Current Opinion in Allergy 

and Clinical Immunology, 4:563-568, 2004.

234. Saxon, A., and Diaz-Sanchez, D. Air Pollution and Allergy: You are what you breathe. Nature 

Immunology, 6:223-6, 2005.

235. Bush RK, Portnoy JM, Saxon A, Terr AI, Wood RA, AAAAI Position Paper: The medical 

effects of mold exposure. J Allergy Clin Immunol.117:326-33, 2006.

236. Zhang K, Zhu D, Kepley C, Terada T, Saxon A. Chimeric human fcgamma-allergen fusion 

proteins in the prevention of allergy. Immunol Allergy Clin North Am. 27:93-103, 2007.

237. Saxon, A, Zhu D, Zhang K, Chan, LA, Kepley, CL Recent advances in the use of genetically 

engineered negative signaling molecules to treat allergic diseases., Arb Paul Ehrlich Inst 

Bundesamt Sera Impfstoffe Frankf A M. 95:223-31, 2006.

238. Zhang K., Behnecke, A., Li. W., Saxon, A. A novel multi-potential dendritic cell targeted gene 

vaccination platform; application to food allergy and beyond. In press. Arb Paul Ehrlich Inst. 

Bundesamt Sera 338-348, 2008.

239. Tsicopoulos, A, Duez, C and Saxon A, Environmental Factors in IgE in Production, in Allergy 

and Allergic Diseases, Volume 1, Second Edition (eds. A.B. Kay, A.P. Kaplan, J. Bousquet and 

P.G Holt), Wiley-Blackwell Publishing Ltd, Oxford, UK, 2009.

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Damp Indoor Spaces

AND HEALTH

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Institute of Medicine (U.S.). Committee on Damp Indoor Spaces and Health.

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 p. ; cm.

 Includes bibliographical references and index.

 ISBN 0-309-09193-4 (hardback)

 1. Indoor air pollution—Health aspects. 2. Dampness in buildings—Health

aspects. 3. Air—Microbiology—Health aspects. 4. Housing and health.

 [DNLM: 1. Air Pollution, Indoor—adverse effects. 2. Air Pollution, Indoor—

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v

COMMITTEE ON DAMP INDOOR SPACES AND HEALTH

Noreen M. Clark, PhD (Chair), Dean, Marshall H. Becker Professor of

Public Health, and Professor of Pediatrics, University of Michigan,

Ann Arbor, Michigan

Harriet M. Ammann, PhD, DABT, Senior Toxicologist, Air Quality

Program, Washington State Department of Ecology, Olympia,

Washington

Bert Brunekreef, PhD, Professor of Environmental Epidemiology, Institute

of Risk Assessment Sciences, University of Utrecht, The Netherlands

Peyton Eggleston, MD, Professor of Pediatrics and Professor of

Environment Health Sciences, Johns Hopkins University, Baltimore,

Maryland

William J. Fisk, MS, PE, Senior Staff Scientist and Department Head,

Indoor Environment Department, Lawrence Berkeley National

Laboratory, Berkeley, California

Robert E. Fullilove, EdD, Associate Dean for Community and Minority

Affairs, Columbia University School of Public Health, New York,

New York

Judith Guernsey, MSc, PhD, Associate Professor, Department of

Community Health and Epidemiology, Dalhousie University, Halifax,

Nova Scotia, Canada

Aino Nevalainen, PhD, Head of Laboratory, Division of Environmental

Health, National Public Health Institute (KTL), Kuopio, Finland

Susanna G. Von Essen, MD, Professor of Pulmonary and Critical Care

Medicine, University of Nebraska Medical Center at Omaha,

Nebraska

Consultants to the Committee

Terry Brennan, MS, President, Camroden Associates, Inc., Westmoreland,

New York

Jeroen Douwes, PhD, Associate Director, Centre for Public Health

Research, Massey University, Wellington, New Zealand

Staff

David A. Butler, PhD, Study Director

Jennifer A. Cohen, Research Associate

Joe A. Esparza, Senior Project Assistant

Elizabeth J. Albrigo, Project Assistant

Norman Grossblatt, Senior Editor

Rose Marie Martinez, ScD, Director, Board on Health Promotion and

Disease Prevention

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vi

This report has been reviewed in draft form by persons chosen for their

diverse perspectives and technical expertise, in accordance with procedures

approved by the National Research Council’s Report Review Committee.

The purpose of this independent review is to provide candid and critical

comments that will assist the institution in making its published report as

sound as possible and to ensure that the report meets institutional standards

of objectivity, evidence, and responsiveness to the study charge. The review

comments and draft manuscript remain confidential to protect the integrity

of the deliberative process. We wish to thank the following for their review

of this report:

Diane R. Gold, MD, MPH, Harvard Medical School and Harvard School

of Public Health

William B. Rose, MArch, School of Architecture, University of Illinois at

Urbana-Champaign

Jonathan M. Samet, MD, Bloomberg School of Public Health, Johns

Hopkins University

Richard J. Shaughnessy, PhD, Indoor Air Program, University of Tulsa

Linda D. Stetzenbach, PhD, Harry Reid Center for Environmental Studies,

University of Nevada, Las Vegas

Mark J. Utell, MD, University of Rochester School of Medicine and

Dentistry

Although the reviewers listed above have provided many constructive

comments and suggestions, they were not asked to endorse the conclusions

or recommendations, nor did they see the final draft of the report before its

release. The review of this report was overseen by Robert B. Wallace, MD,

University of Iowa, and John C. Bailar III, MD, PhD, University of Chicago.

Appointed by the National Research Council and Institute of Medicine, they

were responsible for making certain that an independent examination of

this report was carried out in accordance with institutional procedures and

that all review comments were carefully considered. Responsibility for the

final content of this report rests entirely with the authoring committee and

the institution.

Reviewers

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vii

This report could not have been prepared without the guidance and expertise of numerous persons. Although it is not possible to mention by name

all those who contributed to the committee’s work, the committee wants to

express its gratitude to a number of them for their special contributions.

Sincere thanks go to all the participants at the workshops convened

on March 26, June 17, and October 8, 2002. The intent of the workshops

was to gather information regarding issues related to damp indoor spaces,

health effects attributed to microbial agents found indoors, and mold- and

moisture-related research. The speakers, who are listed in Appendix A, gave

generously of their time and expertise to help inform and guide the committee’s work.

We are deeply indebted to two hard-working people—Terry Brennan

and Jeroen Douwes—who served as consultants and made major contributions to the content of this report. Special thanks are also extended to Harriet

Burge, chair of the committee from its inception through October 2002, for

her exceptional commitment and guidance during her tenure. The committee also thanks Ulla Haverinen-Shaughnessy and Anne Hyvärinen, who permitted excerpting of text from their doctoral dissertations. Institute of Medicine staff members Michelle Catlin, Ben Hamlin, and Michael Schneider

provided valuable input and help over the course of the study. The Committee on Damp Indoor Spaces and Health, of course, takes final responsibility

for all content in the report.

The committee extends special thanks to the dedicated and hard-working staff at the Institute of Medicine (IOM). The expertise and leadership of

Rose Marie Martinez, director of the IOM Board on Health Promotion and

Disease Prevention, helped to ensure that this report met the highest standards of quality.

Finally, the committee would like to thank the chair, Noreen Clark, for

her outstanding work, leadership, and dedication to this project.

Acknowledgments

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ix

Contents

EXECUTIVE SUMMARY 1

Framework and Organization, 2

The Committee’s Evaluation, 4

Reference, 16

1 BACKGROUND AND METHODOLOGIC CONSIDERATIONS 17

Intent and Goals of the Study, 17

Research Approach, 19

Evaluating the Epidemiologic Evidence, 21

Summarizing Conclusions Regarding Epidemiologic Evidence, 26

References, 27

2 DAMP BUILDINGS 29

Moisture Definitions, 30

Moisture Dynamics in Buildings—How Buildings Get Wet, 32

Prevalence, Severity, Location, and Duration of

Building Dampness, 44

Risk Factors for Moisture Problems, 51

From Moisture to Microbial Growth, 54

Microorganisms Occurring in Indoor Spaces and on

Building Materials, 56

Dampness-Related Problems Not Associated with Biologic Sources, 73

Summary, 75

Findings, Recommendations, and Research Needs, 76

References, 78

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x CONTENTS

3 EXPOSURE ASSESSMENT 90

Introduction, 90

Definitions, 91

Sampling Strategies, 94

Assessing Microorganisms, 101

Assessing Microbial Constituents, 103

Assessing Bioallergens, 104

Indirect Exposure-Assessment Methods, 104

Concentrations in the Environment, 110

Evaluation of Exposure Data, 114

Findings, Recommendations, and Research Needs, 115

References, 116

4 TOXIC EFFECTS OF FUNGI AND BACTERIA 125

Considerations in Evaluating the Evidence, 126

Bioavailability and Route of Exposure, 126

Toxic Effects of Indoor Molds and Bacteria, 133

Findings, Recommendations, and Research Needs, 170

References, 171

5 HUMAN HEALTH EFFECTS ASSOCIATED WITH

DAMP INDOOR ENVIRONMENTS 183

Introduction, 183

Evaluating Health Effects, 186

Respiratory Symptoms, 189

Respiratory Tract Disorders, 208

Other Health Complaints and Disorders, 243

Findings, Recommendations, and Research Needs, 253

References, 255

6 PREVENTION AND REMEDIATION OF DAMP

INDOOR ENVIRONMENTS 270

Prevention, 270

Published Guidance for Mold Remediation, 271

Tasks Involved in Remediation, 284

Effects of Air and Surface Cleaning and Ventilation, 301

Findings, Recommendations, and Research Needs, 304

References, 306

7 THE PUBLIC HEALTH RESPONSE 311

Public Health and Housing, 312

Barriers to the Adoption of Dampness Prevention and

Reduction Measures, 313

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CONTENTS xi

Public Health Approaches to Damp Indoor Environments, 314

Findings, Recommendations, and Research Needs, 327

References, 329

APPENDIXES

A WORKSHOP PRESENTATIONS AND SPEAKERS 333

B COMMITTEE, CONSULTANT, AND STAFF BIOGRAPHIES 336

INDEX 343

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1

Executive Summary

A damp spot appears in a ceiling after an intense rainstorm; a hose

loosens from a washing machine, spilling gallons of water onto a basement

floor; weeks after a moldy odor is detected, a plumber finds a slow leak

behind a wall. There are over 119 million housing units in the United States

and nearly 4.7 million commercial buildings (U.S. Census Bureau, 2003),

and almost all of them experience leaks, flooding, or other forms of excessive indoor dampness at some time.

Excessive indoor dampness is not by itself a cause of ill health, but it is

a determinant of the presence or source strength of several potentially

problematic exposures. Damp indoor environments favor house dust mites

and microbial growth, standing water supports cockroach and rodent infestations, and excessive moisture may initiate chemical emissions from building materials and furnishings.

Indoor microbial growth—especially fungal growth—has recently received a great deal of attention in the mass media. It is a prominent feature

of the breakdown of dampness control; its many possible causes include a

breach of the building envelope, failure of a water-use device, and excessive

indoor water-vapor generation. Occupants, health professionals, and others have wondered whether indoor exposure to mold and other agents

might have a role in adverse health outcomes experienced by occupants of

damp buildings. Prominent among these health outcomes is acute idiopathic pulmonary hemorrhage in infants, cases of which were reported in

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2 DAMP INDOOR SPACES AND HEALTH

age and in homes with visible mold (including Stachybotrys chartarum) was

among the risk factors identified in the case infants.

Against that backdrop, the Centers for Disease Control and Prevention

(CDC) asked the Institute of Medicine to convene a committee of experts.

CDC provided the following charge to that committee:

The Institute of Medicine will conduct a comprehensive review of the

scientific literature regarding the relationship between damp or moldy

indoor environments and the manifestation of adverse health effects, particularly respiratory and allergic symptoms. The review will focus on the

non-infectious health effects of fungi, including allergens, mycotoxins and

other biologically active products. In addition, it will make recommendations or suggest guidelines for public health interventions and for future

basic science, clinical, and public health research in these areas.

FRAMEWORK AND ORGANIZATION

Figure ES-1 describes the path by which water or moisture sources may

lead to excessive indoor dampness and to exposures that may result in

adverse health outcomes. The elements of this framework are reflected in

the major topics addressed in the report:

• How and where buildings become wet, the signs of dampness, how

dampness is measured, the risk factors for moisture problems, and what is

known about their prevalence, severity, location, and duration (Chapter 2).

• How dampness influences indoor microbial growth and chemical

emissions, the various agents that may be present in damp environments,

and the influence of building materials on microbial growth and emissions

(Chapter 2).

• The means available for assessing exposure to microorganisms and

microbial agents that occur in damp indoor environments (Chapter 3).

• The experimental data on the nonallergic biologic effects of molds

and bacteria, including the bioavailability of mycotoxins and toxic effects

seen in cellular (in vitro) and animal (in vivo) toxicity studies of mycotoxin

and bacterial toxin exposure (Chapter 4).

• The state of the scientific literature regarding health outcomes and

indoor exposure to dampness and dampness-related agents (Chapter 5).

• Dampness prevention strategies, published guidelines for the removal

of fungal growth (remediation), remediation protocols, and research on the

effectiveness of various cleaning strategies (Chapter 6).

• The public health implications of damp indoor environments and

the elements of a public health response (Chapter 7).

The committee faced a substantial challenge in conducting its review of

these topics—research on fungi and other dampness-related agents is burCopyright 2004 © National Academy of Sciences. All rights reserved.

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EXECUTIVE SUMMARY 3

FIGURE ES-1 A framework describing the potential for water and moisture sources

to lead to excessive indoor dampness and to exposures that may result in adverse

health outcomes.

geoning, and important new papers are constantly being published. Although the committee did its best to paint an accurate picture of the state of

the science at the time its report was completed in late 2003, it is inevitable

that research advances will extend beyond the report’s findings.

External

sources of

water or

moisture

Internal sources

of water or

moisture

 

Accident or breakdown of one or more elements that determine

whether water or moisture sources result in excessive indoor

dampness (component failure; poor building design, construction,

operation, or maintenance; occupant behavior)



Excessive indoor

dampness



Enhanced environment

for house dust mites,

cockroaches, etc.

New or enhanced

growth of mold and

other microbial agents

Dampness-related

degradation of building

materials and

furnishings



Removal processes (ventilation, filtration, surface cleaning, etc.)

that affect indoor pollutant concentrations in air or on surfaces and

the magnitude of potential exposures



Potential exposure of occupants to microbial and

other dampness-related agents

 

Other causes

of health

outcomes



Health

outcome(s)

possibly related

to exposures

No change in

occupant health

status

 

Intervention—elimination of moisture source(s);

remediation; building renovation; changes in

building operation, maintenance and/or occupant

behavior

?

Reduction or elimination of any health outcomes

related to dampness-related exposures

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4 DAMP INDOOR SPACES AND HEALTH

The sections below are a synopsis of the committee’s major findings

and recommendations, and the research needs they identified. Chapters 2–

7 detail the reasoning underlying these and present the committee’s complete findings.

THE COMMITTEE’S EVALUATION

Damp Buildings

The term dampness has been used to define a variety of moisture problems in buildings, including high relative humidity, condensation, water

ponding, and other signs of excess moisture or microbial growth. While

studies report that dampness is prevalent in residential housing in a wide

array of climates, attempts to understand its scale and significance are

hampered by the fact that there is no generally accepted definition of dampness or of what constitutes a “dampness problem.”

There is no single cause of excessive indoor dampness, and the primary

risk factors for it differ across climates, geographic area, and building types.

Although the prevalence of dampness problems appears to increase as buildings age and deteriorate, the experience of building professionals suggests

that some modern construction techniques and materials and the presence

of air-conditioning also increase the risk of dampness problems. The prevalence and nature of dampness problems suggest that what is known about

their causes and prevention is not consistently applied in building design,

construction, maintenance, and use.

One consequence of indoor dampness is new or enhanced growth of

fungi and other microbial agents. The fungi have (eukaryotic) cells like

animals and plants, but are a separate kingdom. Most consist of masses of

filaments, live off of dead or decaying organic matter, and reproduce by

spores. Visible fungal colonies found indoors are commonly called mold or

sometimes mildew. This report, following the convention of much of the

literature on indoor environments, uses the terms fungus and mold interchangeably to refer to the microorganisms.

Mold spores are regularly found in indoor air and on surfaces and

materials—no indoor space is free of them. There are a large number of

species and genera, and those most typically found indoors vary by geographic area, climate, season, and other factors. The availability of moisture is the primary factor that controls mold growth indoors, since the

nutrients and temperature range they need are usually present. While much

attention is focused on mold growth indoors, it is not the only dampnessrelated microbial agent. Mold growth is usually accompanied by bacterial

growth. Some research on fungi and bacteria focuses on specific compoCopyright 2004 © National Academy of Sciences. All rights reserved.

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EXECUTIVE SUMMARY 5

nents that may be responsible for particular health effects: spores and hyphal fragments of fungi, spores and cells of bacteria, allergens of microbial

origin, structural components of fungal and bacterial cells, and such products as microbial volatile organic compounds (MVOCs) and mycotoxins.

Release of these components varies, depending on many physiologic and

environmental factors. Dampness can also damage building materials and

furnishings, causing or exacerbating the release of chemicals and nonbiologic particles from them.

Given the present state of the literature, the committee identified several

kinds of research needs. Standard definitions of dampness, metrics, and associated dampness-assessment protocols need to be developed to characterize

the nature, severity, and spatial extent of dampness. Precise, agreed-on definitions will allow important information to be gathered about the determinants

of dampness problems in buildings and the mechanisms by which dampness

and dampness-related effects and exposures affect occupant health. More

than one definition may be required to meet the specific needs of health

researchers (epidemiologists, physicians, and public-health practitioners) in

contrast with those involved in preventing or remediating dampness (architects, engineers, builders, and those involved in building maintenance). However, definitions should be standardized to the extent possible. Any efforts to

establish common definitions must be international in scope because excessive indoor dampness is a worldwide problem and research cooperation will

promote the generation and dissemination of knowledge.

Research is also needed to better characterize the dampness-related

emissions of fungal spores, bacteria, and other particles of biologic origin

and their role in human health outcomes; the microbial ecology of buildings, that is, the link between dampness, different building materials, microbial growth, and microbial interactions; and dampness-related chemical

emissions from building materials and furnishings, and their role in human

health outcomes. Studies should be conducted to evaluate the effect of the

duration of moisture damage of materials and its possible influence on

occupant health and to evaluate the effectiveness of various changes in

building designs, construction methods, operation, and maintenance in reducing dampness problems. Increased attention should be paid to heating,

ventilation, and air conditioning (HVAC) systems as a potential site for the

growth and dispersal of microbial contaminants that may result in adverse

health effects in building occupants. And research should be performed to

develop designs and construction and maintenance practices for buildings

and HVAC systems that reduce moisture problems; building materials that

are less prone to microbial contamination when moist; and standard, effective protocols for clean-up after flooding and other catastrophic water

events that will minimize microbial growth.

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6 DAMP INDOOR SPACES AND HEALTH

Exposure Assessment

The lack of knowledge regarding the role of microorganisms in the

development and exacerbation of diseases found in occupants of damp

indoor environments is due largely to the lack of valid quantitative exposure-assessment methods and knowledge of which specific microbial agents

may primarily account for the presumed health effects. Very few biomarkers

of exposure to or dose of biologic agents have been identified, and their

validity for exposure assessment in the indoor environment is often not

known. The entire process of fungal-spore aerosolization, transport, deposition, resuspension, and tracking—all of which determine inhalation exposure—is poorly understood, as is the significance of exposures to fungi

through dermal contact and ingestion.

There are several methods for measuring and characterizing fungal

populations, but methods for assessing human exposure to fungal agents

are poorly developed and are a high-priority research need. Part of the

difficulty is related to the large number of fungal species that are measurable indoors and the fact that fungal allergen content and toxic potential

vary among species and among morphologic forms within species. In addition, the most common methods for fungal assessment—counting cultured

colonies and identifying and counting spores—have variable and uncertain

relationships to allergen, toxin, and irritant content of exposures.

Based on their review of the literature, the committee recommends that

existing exposure assessment methods for fungal and other microbial agents

be subjected to rigorous validation and that they be further refined to make

them more suitable for large-scale epidemiologic studies. This includes standardization of protocols for sample collection, transport of samples, extraction procedures, and analytical procedures and reagents. Such work should

result in concise, internationally accepted protocols that will allow measurement results to be compared both within and across studies.

The committee also identified a need to develop improved exposure

assessment methods, particularly methods based on nonculture techniques

and techniques for measuring constituents of microorganisms—allergens,

endotoxins, β(1→3)-glucans, fungal extracellular polysaccharides, fungal

spores, and other particles and emissions of microbial origin. These needs

include further improvement of light and portable personal airborne exposure measurement technology, more rapid development of measurement methods for specific microorganisms that use DNA-based and other

technology, and rapid and direct-reading assays for bioaerosols for the

immediate evaluation of potential health risks. Application of the improved or new methods will allow more valid exposure assessment of

microorganisms and their components, which should facilitate moreinformed risk assessments.

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EXECUTIVE SUMMARY 7

Because only sparse data are available on variation in exposure to

biologic agents in the home environment, it is not possible to recommend

how many samples should be taken to produce an accurate assessment of

risk-relevant exposure.

Toxic Effects of Fungi and Bacteria

Although a great deal of attention has focused on the effects of bacteria

and fungi mediated by allergic responses, these microorganisms also cause

nonallergic responses. Toxicologic studies, which examine such responses

using animal and cellular models, cannot be used by themselves to draw

conclusions about human health effects. However, animal studies are important in identifying hazardous substances, defining their target organs or

systems and their routes of exposure, and elucidating their toxicokinetics

and toxicodynamics, the mechanisms that account for the biologic effects,

metabolism, and excretion of toxic substances. Animal studies are also

useful for generating hypotheses that can be tested through studies of human health outcomes in controlled exposures, clinical studies, or epidemiologic investigations, and they are useful for risk assessment that informs

regulatory and policy decisions.

Research reviewed in Chapter 4 shows that molds that can produce

mycotoxins under the appropriate environmental and competitive conditions can and do grow indoors. Damp indoor spaces may also facilitate the

growth of bacteria that can have toxic and inflammatory effects. Little

information exists on the toxic potential of chemical releases resulting from

dampness-related degradation of building materials, furniture, and the like.

In vitro and in vivo studies have demonstrated adverse effects—including immunotoxic, neurologic, respiratory, and dermal responses—after exposure to specific toxins, bacteria, molds, or their products. Such studies

have established that exposure to microbial toxins can occur via inhalation

and dermal exposure and through ingestion of contaminated food. Animal

studies provide information on the potency of many toxins isolated from

environmental samples and substrates from damp buildings, but the doses

of such toxins required to cause adverse health effects in humans have not

been determined. In vitro and in vivo research on Stachybotrys chartarum

suggests that effects in humans may be biologically plausible, although this

observation requires validation from more extensive research before conclusions can be drawn.

Among the other research needs identified in the chapter is further

development of techniques for detecting and quantifying mycotoxins in

tissues in order to inform questions of interactions and the determination of

exposures resulting in adverse effects. The committee also recommends that

animal studies be initiated to evaluate the effects of long-term (chronic)

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8 DAMP INDOOR SPACES AND HEALTH

exposures to mycotoxins via inhalation. Such studies should establish doseresponse, lowest-observed-adverse-effect levels, and no-observed-adverseeffect levels for identified toxicologic endpoints in order to generate information for risk assessment that is not available from presently-available

studies of acute, high-level exposures.

Human Health Effects Associated with Damp Indoor Environments

The committee used a uniform set of categories to summarize its conclusions regarding the association between health outcomes and exposure

to indoor dampness or the presence of mold or other agents in damp indoor

environments, as listed in Box ES-1. The distinctions among categories

reflect the committee’s judgment of the overall strength, quality, and persuasiveness of the scientific literature evaluated. Chapter 1 details the methodologic considerations underlying the evaluation of epidemiologic evidence

and details the definitions of the categories.

BOX ES-1

Summary of the Categories of Evidence Used in This Report

Sufficient Evidence of a Causal Relationship

Evidence is sufficient to conclude that a causal relationship exists between the

agent and the outcome. That is, the evidence fulfills the criteria for “sufficient evidence of an association” and, in addition, satisfies the following criteria: strength of

association, biologic gradient, consistency of association, biologic plausibility and

coherence, and temporally correct association.

Sufficient Evidence of an Association

Evidence is sufficient to conclude that there is an association. That is, an association between the agent and the outcome has been observed in studies in which

chance, bias, and confounding can be ruled out with reasonable confidence.

Limited or Suggestive Evidence of an Association

Evidence is suggestive of an association between the agent and the outcome

but is limited because chance, bias, and confounding cannot be ruled out with

confidence.

Inadequate or Insufficient Evidence to Determine Whether an

Association Exists

The available studies are of insufficient quality, consistency, or statistical power to permit a conclusion regarding the presence of an association. Alternatively,

no studies exist that examine the relationship.

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EXECUTIVE SUMMARY 9

Tables ES-1 and ES-2 summarize the committee’s findings. The conclusions are not applicable to persons with compromised immune systems,

who are at risk for fungal colonization and opportunistic infections.

Conclusions regarding exposure to agents associated with damp indoor

environments are limited by the means used to assess exposure in the epidemiologic studies reviewed by the committee. For the most part, studies have

relied on occupants’ observations of the presence of “mold” or “moldy

odor.” Relatively few research efforts have used trained observers or measurements to attempt to discern which microbial agents are present, the

extent of their growth, or whether there are specific common potential

exposures (other than dampness). When the committee is drawing a conclusion about the association between exposure to a damp indoor environment and a health outcome, it is not imposing the assumption that the

outcome is necessarily a result of exposure to a particular mold or to

microbial agents in general. In some circumstances, a paper addresses the

association between a particular indoor dampness-related exposure and a

health outcome. However, even in those cases, it is likely that people are

being exposed to multiple agents.

The committee has drawn conclusions about the state of the scientific

literature regarding associations of health outcomes with two circumstances:

TABLE ES-1 Summary of Findings Regarding the Association Between

Health Outcomes and Exposure to Damp Indoor Environmentsa

Sufficient Evidence of a Causal Relationship

(no outcomes met this definition)

Sufficient Evidence of an Association

Upper respiratory (nasal and throat) tract symptoms Wheeze

Cough Asthma symptoms in sensitized

asthmatic persons

Limited or Suggestive Evidence of an Association

Dyspnea (shortness of breath) Asthma development

Lower respiratory illness in otherwise-healthy

children

Inadequate or Insufficient Evidence to Determine Whether an Association Exists

Airflow obstruction (in otherwise-healthy persons) Skin symptoms

Mucous membrane irritation syndrome Gastrointestinal tract problems

Chronic obstructive pulmonary disease Fatigue

Inhalation fevers (nonoccupational exposures) Neuropsychiatric symptoms

Lower respiratory illness in otherwise-healthy adults Cancer

Acute idiopathic pulmonary hemorrhage in infants Reproductive effects

Rheumatologic and other

immune diseases

aThese conclusions are not applicable to immunocompromised persons, who are at increased

risk for fungal colonization or opportunistic infections.

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10 DAMP INDOOR SPACES AND HEALTH

exposure to a damp indoor environment, and the presence of mold or other

agents in a damp indoor environment. As already noted, the term dampness

has been applied to a variety of moisture problems in buildings. Most

of the studies considered by the committee did not specify which agents

were present in the buildings occupied by subjects, and this probably varied

between and even within study populations.

The committee found sufficient evidence of an association between

exposure to damp indoor environments and some respiratory health outcomes: upper respiratory tract (nasal and throat) symptoms, cough, wheeze,

and asthma symptoms in sensitized asthmatic persons. Epidemiologic studies also indicate that there is sufficient evidence to conclude that the presence of mold (otherwise unspecified) indoors is associated with upper respiratory symptoms, cough, wheeze, asthma symptoms in sensitized asthmatic

persons, and hypersensitivity pneumonitis (a relatively rare immune-mediated condition) in susceptible persons.

Limited or suggestive evidence was found for an association between

exposure to damp indoor environments and dypsnea (the medical term for

TABLE ES-2 Summary of Findings Regarding the Association Between

Health Outcomes and the Presence of Mold or Other Agents in Damp

Indoor Environmentsa

Sufficient Evidence of a Causal Relationship

(no outcomes met this definition)

Sufficient Evidence of an Association

Upper respiratory (nasal and throat) tract symptoms Wheeze

Asthma symptoms in sensitized asthmatic persons Cough

Hypersensitivity pneumonitis in susceptible personsb

Limited or Suggestive Evidence of an Association

Lower respiratory illness in otherwise-healthy children

Inadequate or Insufficient Evidence to Determine Whether an Association Exists

Dyspnea (shortness of breath) Skin symptoms

Airflow obstruction (in otherwise-healthy persons) Asthma development

Mucous membrane irritation syndrome Gastrointestinal tract problems

Chronic obstructive pulmonary disease Fatigue

Inhalation fevers (nonoccupational exposures) Neuropsychiatric symptoms

Lower respiratory illness in otherwise-healthy adults Cancer

Rheumatologic and other immune diseases Reproductive effects

Acute idiopathic pulmonary hemorrhage in infants

aThese conclusions are not applicable to immunocompromised persons, who are at increased

risk for fungal colonization or opportunistic infections.

bFor mold or bacteria in damp indoor environments.

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EXECUTIVE SUMMARY 11

shortness of breath), lower respiratory illness in otherwise-healthy children,

and the development of asthma in susceptible persons. It is not clear whether

the latter association reflects exposure to fungi or bacteria or their constituents and emissions, to other exposures related to damp indoor environments, such as dust mites and cockroaches, or to some combination thereof.

The responsible factors may vary among individuals. For the presence

of mold (otherwise unspecified) indoors, there is limited or suggestive

evidence of an association with lower respiratory illness in otherwise-healthy

children.

Inadequate or insufficient information was identified to determine

whether damp indoor environments or the agents associated with them are

related to a variety of health outcomes listed in Tables ES-1 and -2. Included among these is acute idiopathic pulmonary hemorrhage in infants

(AIPHI). The committee concluded that the available case-report information constitutes inadequate or insufficient information to determine whether

an association exists between AIPHI and the presence of Stachybotrys

chartarum or exposure to damp indoor environments in general. AIPHI is a

serious health outcome, and the committee encourages the CDC to pursue

surveillance and additional research on the issue to resolve outstanding

questions.

The committee considered whether any of the health outcomes listed

above met the definitions for the categories “sufficient evidence of a causal

relationship” and “limited or suggestive evidence of no association” defined in Chapter 1, and concluded that none did.

It offers some additional observations on research needs and recommendations for action:

• Indoor environments subject occupants to multiple exposures that

may interact physically or chemically with one another and with the other

characteristics of the environment, such as humidity, temperature, and ventilation rate. Few studies to date have considered whether there are additive

or synergistic interactions among these factors. The committee encourages

researchers to collect and analyze data on a broad range of exposures and

factors characterizing indoor environments in order to inform these questions and possibly point the way toward more effective and efficient intervention strategies.

• The committee encourages the CDC to pursue surveillance and additional research on acute pulmonary hemorrhage or hemosiderosis in infants

to resolve questions regarding this serious health outcome. Epidemiologic

and case studies should take a broad-based approach to gathering and

evaluating information on exposures and other factors that would help to

elucidate the etiology of acute pulmonary hemorrhage or hemosiderosis

in infants, including dampness and agents associated with damp indoor

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12 DAMP INDOOR SPACES AND HEALTH

environments; environmental tobacco smoke (ETS) and other potentially

adverse exposures; and social and cultural circumstances, race/ethnicity,

housing conditions, and other determinants of study subjects’ health.

• Concentrations of organic dust consistent with the development of

organic dust toxic syndrome are very unlikely to be found in homes or

public buildings. However, clinicians should consider the syndrome as a

possible explanation of symptoms experienced by some occupants of highly

contaminated indoor environments.

• Greater research attention to the possible role of damp indoor environments and the agents associated with them in less well understood

disease entities is needed to address gaps in scientific knowledge and concerns among the public.

Prevention and Remediation of Damp Indoor Environments

Homes and other buildings should be designed, operated, and maintained to prevent water intrusion and excessive moisture accumulation

when possible. When water intrusion or moisture accumulation is discovered, the source should be identified and eliminated as soon as practicable

to reduce the possibility of problematic microbial growth and buildingmaterial degradation. The most effective way to manage microbial contaminants, such as mold, that are the result of damp indoor environments is

to eliminate or limit the conditions that foster its establishment and growth.

That also restricts the dampness-related degradation of building materials

and furnishings.

Information is available on the sources of excessive indoor dampness

and on the remediation of damp indoor conditions and its adverse consequences. Chapter 6 summarizes several sources of guidance on how to

respond to various indoor microbial contamination situations. However, as

the committee observes, determining when a remediation effort is warranted or when it is successful is necessarily subjective because there are no

generally accepted health-based standards for acceptable concentrations of

fungal spores, hyphae, or metabolites in the air or on surfaces.

There is a great deal of uncertainty and variability in samples of mold

and other microbial materials taken from indoor air and surfaces, but the

information gained from a careful and complete survey may aid in the

evaluation of contamination sources and remediation needs. Visible surfaces and easily accessible spaces are not the only source of microbial

contaminants, however, and the potential for exposure from sources in

spaces such as attics, crawl spaces, wall cavities, and other hidden or seldomaccessed areas is poorly understood.

When microbial contamination is found, it should be eliminated by

means that not only limit the possibility of recurrence but also limit expoCopyright 2004 © National Academy of Sciences. All rights reserved.

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EXECUTIVE SUMMARY 13

sure of occupants and persons conducting the remediation. Disturbance of

contaminated material during remediation activities can release microbial

particles and result in contamination of clean areas and exposure of occupants and remediation workers. Containment during clean-up (through the

erection of barriers, application of negative air pressure, and other means)

has been shown to prevent the spread of microbial particles to noncontaminated parts of a contaminated building. The amount of containment

and worker personal protection and the determination of whether occupant

evacuation is appropriate depend on the magnitude of contamination.

Notwithstanding the interest in the topic, very few controlled studies

have been conducted on the effectiveness of remediation actions in eliminating problematic microbial contamination in the short and long term or

on the effect of remediation actions on the health of building occupants. In

addition, the available literature addresses the management of microbial

contamination when remediation is technically and economically feasible.

There is no literature addressing situations where intervening in the moisture

dynamic or cleaning or removing contaminated materials is not practicable.

Among the research needs identified by the committee are studies that

better characterize the effectiveness of remediation assessment and remediation methods in different contamination circumstances, the dynamics of

movements of contaminants from colonies of mold and other microorganisms in spaces such as attics, crawl spaces, exterior sheathing, and garages,

and the effectiveness of various means of protection of workers and occupants during remediation activities. Standard methods should be formulated

to assess the potential of new materials, designs, and construction practices to

cause or exacerbate dampness problems. And research should be performed

to address the other data gaps discussed above and to determine

• How free of microbial contamination a surface or building material

must be to eliminate problematic exposure of occupants and in particular,

how concentrations of microbial contamination left after remediation are

related to those found on ordinary surfaces and materials in buildings where

no problematic contamination is present.

• Whether and when microbial contamination that is not visible

to the naked eye but is detectable through screening methods should be

remediated.

• The best ways to open a wall or other building cavity to seek hidden

contamination while controlling the release of spores, microbial fragments,

and the like.

• The effectiveness of managing contamination in place by using negative air pressure, encapsulation, and other means of isolation.

• How to measure the effectiveness and health effects of a remediation

effort.

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14 DAMP INDOOR SPACES AND HEALTH

The Public Health Response

On the basis of its review of the scientific papers and other information summarized above and detailed in the report, the committee concludes that excessive indoor dampness is a public-health problem. An

appropriate public health goal should thus be to prevent or reduce the

incidence of potentially problematic damp indoor environments, that is,

environments that may be associated with undesirable health effects, particularly in vulnerable populations. However, there are serious challenges

associated with achieving that goal. As the report indicates, there is insufficient information on which to base quantitative recommendations for

either the appropriate level of dampness reduction or the “safe” level of

exposure to dampness-related agents. The relationship between dampness

or particular dampness-related agents and health effects is sometimes

unclear and in many cases indirect. Questions of exposure and dose have

not, by and large, been resolved. It is also not possible to objectively rank

dampness-related health problems within the larger context of threats to

the public’s health because there is insufficient information available to

confidently quantify the overall magnitude of the risk resulting from exposures in damp indoor environments.

Institutional and social barriers may hinder the widespread adoption of

technical measures and practices that could prevent or reduce problematic

indoor dampness. Economic factors, for example, encourage poor practice

or impede remediations; they may also create incentives to forgo or limit

investment in maintenance that might help to prevent moisture problems.

Given these challenges, the committee identifies seven areas of endeavor

that deserve discussion in the formulation of public health mechanisms to

prevent or reduce the incidence of damp indoor environments:

• Assessment and monitoring of indoor environments at risk for problematic dampness.

• Modification of regulations, building codes, and building-related

contracts to promote healthy indoor environments; and enforcement of

existing rules.

• Creation of incentives to construct and maintain healthy indoor

environments; and financial assistance for remediation where needed.

• Development, dissemination, and implementation of guidelines for

the prevention of dampness-related problems.

• Public-health-oriented research and demonstration projects to evaluate the short-term and long-term effectiveness of intervention strategies.

• Education and training of building occupants, health professionals,

and people involved in the design, construction, management, and mainteCopyright 2004 © National Academy of Sciences. All rights reserved.

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EXECUTIVE SUMMARY 15

nance of buildings to improve efforts to avoid or reduce dampness and

dampness-related health risks.

• Collaborations among stakeholders to achieve healthier indoor

environments.

Among the recommendations the committee offers for implementing

the actions it suggests are these:

• CDC, other public-health-related, and building-managementrelated funders should provide new or continuing support for research

and demonstration projects that address the potential and relative benefit

of various strategies for the prevention or reduction of damp indoor

environments, including data acquisition through assessment and monitoring, building code modification or enhanced enforcement, contract

language changes, economic and other incentives, and education and training. These projects should include assessments of the economic effects of

preventing building dampness and repairing damp buildings and should

evaluate the savings generated from reductions in morbidity and gains in

the useful life of structures and their components associated with such

interventions.

• Carefully designed and controlled longitudinal research should be

undertaken to assess the effects of population-based housing interventions

on dampness and to identify effective and efficient strategies. As part of

such studies, attention should be paid to definitions of dampness and to

measures of effect; and the extent to which interventions are associated

with decreased occurrence of specific negative health conditions should be

assessed when possible.

• Government agencies with housing-management responsibility should

evaluate the benefit of adopting economic-incentive programs designed to

reward actions that prevent or reduce building dampness. Ideally, these should

be coupled with independent assessments of effectiveness.

• HUD or another appropriate government agency with responsibility

for building issues should provide support for the development and dissemination of consensus guidelines on building design, construction, operation, and maintenance for prevention of dampness problems. Development

of the guidelines should take place at the national level and should be under

the aegis of either a government body or an independent nongovernment

organization that is not affiliated with the stakeholders on the issue.

• CDC and other public-health-related funders should provide new or

continuing support for research and demonstration projects that:

— Develop communication instruments to disseminate information

derived from the scientific evidence base regarding indoor dampness, mold

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16 DAMP INDOOR SPACES AND HEALTH

and other dampness-related exposures, and health outcomes to address

public concerns about the risk from dampness-related exposures, indoor

conditions, and causes of ill health.

— Foster education and training for clinicians and publichealth professionals on the potential health implications of damp indoor

environments.

• Government and private entities with building design, construction,

and management interests should provide new or continuing support for

research and demonstration projects that develop education and training

for building professionals (architects, home builders, facility managers and

maintenance staff, code officials, and insurers) on how and why dampness

problems occur and how to prevent them.

• Those formulating the education and training programs discussed

above should include means of evaluating whether their programs are reaching relevant persons and, ideally, whether they materially affect the occurrence of moisture or microbial contamination in buildings or occupant

health.

REFERENCE

U.S. Census Bureau. 2003. Statistical Abstract of the United States 2002. United States Department of Commerce.

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Exhibit 3

Case: 1:17-cv-00695-MRB Doc #: 65-3 Filed: 05/20/19 Page: 66 of 81 PAGEID #: 2335
Andrew Saxon, MD, Professor, Emeritus Chief

Clinical Immunology/Allergy

Department of Medicine, 52-262 CHS

David Geffen School of Medicine at UCLA

University of California, Los Angeles

Los Angeles, California 90095-1690

310-367-9736, 310-206-8622 (Fax)

asaxon@mednet.ulca.edu

Page 1

REPORT OF ANDREW SAXON, M.D.

RE: Ms. Beckemeyer vs GELCO

I. QUALIFICATIONS

My name is Andrew Saxon, M.D. I am a licensed physician in the State of California 

specializing in the area of Clinical Immunology & Allergy. I am the founder and emeritus chief 

of the Division of Clinical Immunology and Allergy at the UCLA School of Medicine, Los 

Angeles, California. I am currently a Professor of Medicine at the David Geffen School of 

Medicine at UCLA.

I received my medical degree from Harvard Medical School in Boston, Massachusetts, in 

1972. I completed my residency in internal medicine at Harbor General Hospital in Los 

Angeles, California, in 1975, and my post-doctoral training in immunology in the Department of 

Microbiology and Immunology at the UCLA School of Medicine in 1977. I am a licensed 

physician in California through the National Board of Medical Examiners. I am board certified in 

(1) Internal Medicine by the American Board of Internal Medicine, (2) Allergy and Immunology 

by the American Board of Allergy and Immunology, and (3) Diagnostic Laboratory Immunology 

by the American Board of Diagnostic Laboratory Immunology. I founded the Division of 

Clinical Immunology and Allergy in the Department of Medicine at UCLA in 1977 and served 

as its Chairman for 30 years. I also founded the UCLA Asthma, Allergy, and Immunologic 

Disease Center and served as Director until the time of my retirement. I have published over 

190 scientific papers in peer-reviewed journals in the field of immunology and I provide many 

editorial/review services for such journals including for over a decade being Editor in Chief of 

Clinical Immunology, the official journal of the Clinical Immunology Society. I also have served 

on peer-review funding committees for the National Institutes of Health and other organizations 

as well as chair the Allergy/Asthma section of the Immune Tolerance Network, a major 

undertaking by the National Institutes of Health and private institutions to discover true cures 

for immune mediated disorders. 

I am a co-author of the American College of Occupational & Environment Medicine (ACOEM) 

original Position Statement entitled: Adverse Human Health Effects Associated with Molds in 

the Indoor Environment that appeared in 2002. ACOEM represents more than 6,000 

physicians and other health care professionals and is the nation's largest medical society of 

individuals specializing in the field of occupational and environmental medicine. I am also a coauthor of the American Academy of Allergy Asthma and Immunology’s (AAAAI) official Position 

statement entitled “The Health Effects of Molds” which appeared in 2006. The AAAAI, with 

over 5000 members, is the nation’s largest medical subspecialty society specifically dealing 

with the allergic and immune aspects of mold exposures.

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Further elaboration of my professional background, prior publications and credentials is given 

in the attached true and correct copy of my curriculum vitae and bibliography (Attachment 

“A”). 

II. DATA RELIED UPON

A. The basis of my testimony includes my education, clinical and basic science training, 

experience, and review of both basic and clinical studies regarding humans and the 

immune system. This includes basic studies performed in the test tube and in animals 

regarding mold and related substances, my own research in human and animal immune 

reactivity, review of the exhibits, depositions and opinions of identified plaintiff experts, 

my extensive reading in the areas of immunology which includes allergy, autoimmunity, 

cancer of the immune system (lymphomas), and related areas, and my clinical 

experience including the diagnosis and management of patients with immunologically 

related disorders.

B. Included in this is extensive analysis of the literature relating to mold/fungal related 

illness in humans including the Institute of Medicine’s 2004 Publication “Damp indoor 

spaces and Health” (Executive Summary provided as Attachment “B”), the American 

College of Medical Toxicology’s Statement in Support of the Institute of Medicine’s 

report (Attachment “C”) and the 2009 World Health Organization (2009) Guidelines for 

Indoor Air Quality (Executive Summary provided as Attachment “D”)..I am also relying 

upon the 2018 German review (Attachment E), the 2017 review by Borchers and 

Gershwin (Attachment “F”), the Position Statement of the American College of 

Occupational and Environmental Medicine promulgated by the Society in 2011 

(Attachment “G”) and the 2006 Position Statement of the American Academy of 

Allergy, Asthma and Immunology, Asthma and Immunology (Attachment “H”.) I have 

also analyzed the 2008 General Accounting Office document entitled “Indoor Mold: 

Better Coordination of Research on Health Effects and More Consistent Guidance

Would Improve Federal Efforts.” (Attachment “I”.)

C. I am also relying upon my analysis of the case-specific materials provided to me. This 

includes:

C1. Medical records of the plaintiff Melanie Ann Beckemeyer PharmD from the following 

sources that span the timeframe March 2001 through July 2018.

• Allergy and Asthma Specialty Group. 

• Bernstein Allergy Group. 

• Bethesda Alcohol and Drug Treatment (no records) 

• Huber personalized medicine (Dr. Gray Huber, Integrative Medicine)

• Kroger Little Clinic.

• Liberty Urgent Care. 

• Dr. Harold T. Pretorius. 

• Plaintiff produced 2315 pages of medical documents that include the records of 

Dr. Craig P. Cleveland.

• Blue Ash Family Medicine

• Report of Richard Sexton, PhD of April 2017.

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Saxon Rule Report in Beckemeyer vs GELCO Page 3 of 15

C2. Environmental records

• The Report of Jeremy Porter, PMP dated 11.6.18

• Report from Ecostratum dated 7.25.18 for vehicle testing on 7.9.18

C3. Legal Documents

• Complaint filed in this matter.

• Discovery responses filed in this matter

• Depositions of Ms. Melanie Beckemeyer, PharmD. dated 9.27.18 and 11.5.18

• Expert Report of Dr. Scott McMahon in Beckemeyer vs. GELCO 8.31.18

• Expert Report of Dr. Scott McMahon in Fleming v Baker 3.29.17 (Attachment

“J”)

• Deposition Testimony of Dr. Scott McMahon in Fleming v Baker 4.7.17

(Attachment “K”)

• Depositions of Scott W. McMahan in Courcelle v. CW NOLA PROPERTIES 

dated 8.18.17 and 5.18.18 Attachment “L”)

• Declaration Of Scott W. Mc Mahon, MD in Courcelle v. CW NOLA Properties 

Dated 8.15.17

• United States District Court Western District of Washington At Seattle, Court 

order 16356136 dated 8.13.15 in Haneet Kumar, et al., v. Williams Portfolio 7, 

Inc. (Attachment “K”)

III. OPINIONS

IIIA. Opinions about Plaintiff, Ms. Melanie Ann Beckemeyer, PharmD.

Background: In this section, I will address Ms. Beckemeyer’s actual medical conditions as 

shown by the evidence in her medical records. By way of timeframe, Ms. Beckemeyer was in 

possession of the vehicle in question from May 4, 2016 through September 30, 2016. She 

reported to her doctor that the last time she was in the car was September 23, 2016.

Ms. Melanie Beckemeyer, date of birth 6.5.58. Ms. Beckemeyer is 60-year old woman. She 

was reported to be 5’7’ tall and weighed 145 lbs. on 6.26.17, the last weight I see recorded. 

Her medical records state that she is a non-smoker and that she would drink two to four 

alcoholic beverages/week. The medical records relating to Ms. Beckemeyer indicate to me that 

she has the following medical issues:

Hypertension- high blood pressure with secondary cognitive Issues due to small vessel 

ischemic changes. 

Ms. Beckemeyer has had high blood pressure for many years. She was reported to have 

hypertension in 2001 in her first available medical record. She has been maintained on antiCase: 1:17-cv-00695-MRB Doc #: 65-3 Filed: 05/20/19 Page: 69 of 81 PAGEID #: 2338
Saxon Rule Report in Beckemeyer vs GELCO Page 4 of 15

hypertensive medication (Irbesartan most recently) for a number of years and was taking that 

medication at the time of her 11.5.18 deposition. Common side effects of Irbesartan include 

dizziness, fatigue, indigestion, diarrhea and heartburn. She reported no renal disease, 

coronary artery disease or stroke related to her hypertension.. However, a MRI of her brain on 

6.13.17 showed “microangiopathic white matter disease consistent with chronic small vessel 

ischemia, most often seen in manifestation of hypertensive atherosclerosis or metabolic 

factors.” There was also mild right greater than left hippocampal atrophy that potentially may 

correlate with memory symptoms possibly related to early manifestation of mild cognitive 

impairment syndrome. A NeuroQuant study the same day was read as normal. Ms. 

Beckemeyer’s records reflect she has been having concerns about her cognitive abilities since 

sometime in 2016. She referred herself to a neuropsychologist, Richard Sexton, PhD who saw 

her in May of 2017. He reported that; “Overall, the results of the present assessment

suggested that Dr. Beckemeyer is a person of above average intellectual abilities, who

maintains overall cognitive/functional integrity. She demonstrated relative strengths in

conceptualization, visual-spatial construction, attention, and non-verbal immediate and shortterm ("working") memory/reasoning, as well as naming. She demonstrated relative

weaknesses in orally-presented words/stories, delayed visual/spatial and verbal recall, and

rote verbal repetition in immediate-, short-, and long-term aspects. Based onher educational

and occupational/vocational history, it might be inferred that her pattern of performance

might reflect a reduction from premorbid levels in the areas noted above. It is not the general

pattern observed in the normal aging process or related to any emotional factor, as any

reported symptoms (e.g. anxiety) were not at a disabling level. The pattern would appear to

reflect the impact of vascular brain changes (emphasis added) or the possibility of

neurotoxin exposure.”

Assessment and opinion. 

It is my opinion that Ms. Beckemeyer has long-standing hypertension with underlying 

microvascular CNS changes resulting in a mild impairment of certain cognitive functions. Long 

standing hypertension with secondary microvascular changes is a very common scenario in a 

63-year-old person. In contrast, exposures to molds, bacteria and their byproducts such as Ms. 

Beckemeyer may have had in the car in question or anywhere else are not going to involve 

exposure to direct neurotoxins to any significant degree. Another factor driving in Ms. 

Beckemeyer’s cognitive complaints is her response to anxiety/stress as discussed below.

Upper Respiratory and external ocular symptoms: Allergic Rhinitis & Allergic Conjunctivitis, 

Ms. Beckemeyer has seen an allergist, Dr. Ahmad since 2001. When he first saw her, she told 

him she had had “allergies” for more than 10 years. Ms. Beckemeyer had allergy testing by 

Dr. Ahmad in 2004. The only testing results in the records from 2004are those from

intradermal testing that showed weakly positive tests to dust mites, cat, dog and “mold 2”. 

While “prick tests are “circled” and presumably done at some point before the intradermal 

tests, no results of prick testing is available. Ms. Beckemeyer stated in her deposition that she 

received 3-4 years of allergy immunotherapy injections from Dr. Ahmad. The records of those 

injections and their composition is not in Dr. Ahmad’s records that I received. Dr. Ahmad saw 

Ms. Beckemeyer on again in February 2012 and then again in 2016. He had Ms. Beckemeyer 

undergo allergy testing on 12.27.16. Thirty eight allergy Prick tests were done and only 

Epicoccum and Fusarium were recorded as “positive “at 3+ with soy at 1+ and peanut was 

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Saxon Rule Report in Beckemeyer vs GELCO Page 5 of 15

read as 1-2+. However, there is no reading scale for these tests nor is there a positive 

(histamine) or negative (saline) control result provided. Intradermal testing on that date was 

read as 1+ to cat and dog, 2+ to Molds 2 and 0 to Molds 1. Ms. Beckemeyer’s records do not 

give any evidence of her having asthma. Ms. Beckemeyer has never been heard to wheeze in 

spite of multiple physical examinations of her lungs nor has any doctor even suggested she 

undergo breathing tests to look into this issue. While a number of medical records say she has 

“asthma”, others say she does not. Ms. Beckemeyer herself testified in her deposition that she 

does not have asthma.

Assessment and Opinion. 

It is my opinion that the data is unclear whether Ms. Beckemeyer is an allergic (atopic) person 

with allergic rhinitis and allergic conjunctivitis. Her history and physical examinations would

indicate that is a reasonable diagnosis. However, the testing by Dr. Ahmad is problematic. The 

accurate form of allergy skin testing is prick testing while intradermal testing is fraught with the 

problem of false positive tests and particularly so in the face of multiple negative prick tests. 

The records I have only contain Ms. Beckemeyer’s 2004 intradermal allergy skin testing, not 

her prick test results. However, it is reasonable to assume that the prick tests for molds, 

pollens, dust mites and animal dander were negative for one would never do intradermal 

testing to allergens that were positive on prick testing. The sets of allergy tests in December 

2016 have no controls and provide no reading scales. Here the only “positive” prick tests were 

Epicoccum and Fusarium.

It is my opinion that, given the flaws in Dr. Ahmad’s testing, I would not rely upon them to make 

medical diagnosis of inhalant allergy or to exclude it. I would recommend Ms. Beckemeyer 

gets reliable allergy blood testing done with the ImmunoCap II or equivalent third generation of 

allergy blood testing to determine what, if any, allergens she is allergic to. 

It is my opinion that even if Ms. Beckemeyer is an allergic subject and the testing at Dr. 

Ahmad’s office is accurate, the only allergens identified by the prick testing were Epicoccum 

and Fusarium and her exposure to these in the vehicle in question would have been far less 

than her exposure from outside air as discussed in Mr. Porter’s report. 

It is my opinion that Ms. Beckemeyer does not have asthma, allergic or otherwise.

Status post turbonectomy and septoplasty. Ms. Beckemeyer reports that she underwent a 

nasal turbonectomy and septoplasty prior to 2001. The reasons and date for this surgery are 

not elucidated in the medical records. 

Assessment and opinion

It is my opinion that Ms. Beckemeyer’s turbonectomy and septoplasty would have be related to 

cosmesis, anatomic nasal obstruction and her rhinitis (allergic or otherwise) which is discussed 

above..

Anxiety, Panic Attacks and Depression.

Ms. Beckemeyer records from Blue Ash Family Medicine document that she has had problems

with depression, anxiety and panic attacks since 2011. Ms. Beckemeyer reported to those 

doctors that her stress in 2011 was related to both her job and her personal life. She was 

begun on Celexa, an antidepressant on September 8, 2011. When seen on September 26, 

2011, she reported she felt that “she cannot complete tasks that require organization and 

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higher levels of cognition in a reasonable amount of time due to ongoing anxiety.” She 

remained on Celexa, through 7.1.16 and was to continue it according to the records but the 

note from 9.7.16 does not include Celexa in the medications she is taking. The records are

silent whether Beckemeyer was advised to stop Celexa by her physicians or if she stopped it

on her own. Ms. Beckemeyer did not identify Celexa as a medication she was taking at the 

time of her deposition on 11.5.18. Ms. Beckemeyer had taken Xanax, an anxiolytic in the 

1990’s. She testified in her deposition that she was taking Xanax for dizziness and balance 

issues she was having at the time and in fact, illegally wrote herself a prescription for this drug 

which resulted in her being arrested and having her pharmacy license revoked for a time. 

By mid 2017, Ms. Beckemeyer had developed a whole panoply of ongoing symptoms that she 

felt were related to her exposure to the vehicle in question which ended the previous 

September, The symptoms she reported on 7.5.17 included disturbed sleep, fatigue, joint 

pain/swelling, bladder problems, buzzing/ringing/ear pain, ,blurry vision, disorientation,

forgetfulness, loss of libido, unexplained hair loss, vertigo, confusion, difficulty with 

concentration, and swollen glands. She endorsed mood swings/irritability/depression at that 

time as well. 

Assessment and Opinion.

It is my opinion that Ms. Beckemeyer has a generalized anxiety disorder with panic attacks and 

major depressive illness. Notably, when anxious in the past, she reported cognitive symptoms 

very similar to what she reports now. It is my opinion that her anxiety/mood issues color and 

magnify her symptoms, e.g. fatigue from medications, cognitive changes etc. as well drive 

such symptoms on their own as such mood issues do in all patients. It is notable Ms. 

Beckemeyer was no longer taking her antidepressant medication in the timeframe that she 

began to report the increasing number of somatic symptoms, she now believes were due to 

exposure mold in the vehicle in question. It is my opinion that Ms. Beckemeyer likely has

developed a somatic symptom disorder focused on her belief about the injury she received 

from her mold exposure in the vehicle in question. 

Vertigo/disequilibrium/dizziness: 

Ms. Beckemeyer reports she first had problems with vertigo and disequilibrium when she was 

diagnosed with Meniere’s disease in her 30s. She says that she underwent endolymphatic sac 

surgery, reportedly in 1997, and had resolution of those symptoms. Those records are not 

available to me. On 9.18.15, Ms. Beckemeyer saw her primary care physician for ear pressure 

and being off balance that she described as feeling “swimmy.” She did not report true vertigo. 

She also complained of nausea. At that visit, she requested a letter from the doctor to her 

employer as she reported that the employer arranged shuttle from the airport was causing 

nausea. She was treated with a short course of prednisone and a nasal steroid for presumed

eustachian tube dysfunction. On 9.29.15, Ms. Beckemeyer was seen in urgent care 

complaining of problems with wooziness and vertigo that she attributed to have neck 

manipulation for Temporal Mandibular Joint (TMJ) issues. She was found to lateralize 

translational movements to the left on tandem positioning. Then in September of 2016, she 

complained of increasing light-headedness and dizziness. Over the ensuring months, she had 

an extensive work up for this including a neuro-otology consultation and no specific etiology 

was found for her ongoing complaints of light-headedness and dizziness. These symptoms 

persisted through the middle of 2017 at least. 

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Assessment and Opinion.

It is my opinion that Ms. Beckemeyer’s more recent complaints of feeling dizzy and 

lightheaded are most likely a manifestation of both her microvascular CNS disease that is 

secondary to her long standing hypertension and her anxiety/stress.

Treatment with thyroid hormone Ms. Beckemeyer has been on thyroid hormone replacement 

medication for many years. She said in her deposition that she was started on “glandular 

thyroid” because someone felt she was low on thyroid. It is not clear in the records when she 

first started taking thyroid hormone medication nor is it clear why she was placed on it. Her 

anti-thyroid antibodies were negative indicating she does not have autoimmune thyroiditis, the 

most common cause of hypothyroidism. Ms. Beckemeyer’s medical records also show that in 

2017 she was taking too much thyroid hormone as documented by her very low TSH levels. 

Her most recent TSH level in 7.26.18 was normal.

Assessment and Opinion.

It is my opinion that if Ms. Beckemeyer actually does have underlying thyroid disease, which is 

not evident, it was pre-existing and any thyroid issues she may have are not related to 

exposure to mold, mold byproducts or ambient bacteria. It is also my opinion that 

overtreatment with thyroid hormone as in 2017 would exacerbate both her hypertension and 

her anxiety and have other potential longer-term adverse health effects. 

Polycystic Ovary Syndrome with insulin resistance. Ms. Beckemeyer reported that she had

been diagnosed with polycystic ovary syndrome and associated insulin resistance prior to 

2012. There is no information to verify this diagnosis in the available medical records. Her 

records also document she has been treated with Metformin for this condition for many years.

She was on metformin at the time of her deposition on 11.5.18. Her records do not give 

evidence of hyperglycemia or diabetes.

Assessment and Opinion. It is my opinion that should Ms. Beckemeyer have polycystic ovary 

syndrome; it was pre-existing and that condition is not related to exposure to mold, mold 

byproducts or ambient bacteria.

Glaucoma, reportedly “familial.” Ms. Beckemeyer’s medical records report that on 6.12.14 she 

reported that she had been seen for glaucoma and she stated this was “familial” There is no 

other information about this issue in her records. 

Assessment and Opinion. It is my opinion that if Ms. Beckemeyer has glaucoma, familial or 

otherwise, it is unrelated to exposure to mold, mold byproducts or ambient bacteria. 

Alternative health care and the pseudo-diagnosis of Chronic Inflammatory Response 

Syndrome, aka “CIRS.” Ms. Beckemeyer has sought out a set of alternative health care 

providers such as Drs. Huber, Cleveland and Shoemaker/McMahon for an increasing panoply 

of symptoms that have persisted well after her alleged exposure ended. She has done so by 

self-referral as she testified to in her deposition. 

Assessment and Opinion. It is my opinion that, as discussed earlier, Ms. Beckemeyer has a 

number of medical conditions including well-recognized psychiatric issues that contribute to 

her overall set of complaints. However, Ms. Beckemeyer, a PharmD. who would not be 

expected to be naïve in terms of what is generally accepted vs alternative/fringe medical care, 

has sought out medical practitioners who practice alternative/fringe medicine. Ms. 

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Beckemeyer self-referred herself to Dr. Huber who endorses “Shoemaker testing”, Dr. 

Cleveland who gave her nystatin for “mold exposure” and then sought out Dr. Shoemaker who 

referred her to his “trainee”, Dr. McMahon. This issue of her fringe medical care is discussed 

below in Section IIID below.

IIIB. Opinions re mechanisms of adverse health effects from exposure to mold/mold 

products in the home and office setting as related to the plaintiff, Ms. 

Beckemeyer. 

Adverse health effects from mold and their byproducts occur via three main mechanisms, 

Immune, Infectious and Toxic/irritant (all discussed in detail in Attachments “B” through 

“H”). Each of these can be addressed in terms of whether Ms. Beckemeyer had/has evidence 

for an adverse health effect from mold.

i. Immune effects: There are three main possible immune mediated diseases to consider.

First is typical inhalant allergy that induces allergic rhinitis and allergic asthma. Ms. 

Beckemeyer’s respiratory issues were discussed in detail earlier so I will not repeat that 

analysis here. Essentially, the medical data regarding Ms. Beckemeyer indicate she 

may be one of the 10% of the population who has allergic sensitization to a variety of 

aeroallergens including molds. However, even if she were to be, her exposure in the 

vehicle in question would not be the source of allergic symptoms compared to regular 

outdoor air. The other forms of known immune adverse health effect from exposure to 

mold or mold byproducts are rare conditions known as allergic bronchopulmonary 

aspergillosis (ABPA) and hypersensitivity pneumonitis, There is no indication of Ms. 

Beckemeyer having these rare illnesses.

ii. Infection: Ms. Beckemeyer has had no mold infections. In fact, the records do not even 

reflect that she has had problems of mold infections that are common in the general 

population such as mold toenail infections or skin infections. I would add that oral or 

vaginal candida infections are due to a yeast, Candida albicans and is not due to a 

mold. That yeast is resident on normal mucosal surfaces in humans but overgrows to 

become an infection under a variety of circumstances unrelated to ambient

environmental conditions.

iii. Toxic/Irritant effects

a. Toxic effects. As discussed in Attachments B-H, M and N, toxic effects from 

inhalation of mold spores or other microbial agents in a residential setting or the vehicle 

in question essentially do not occur. This is simply a result of dose considerations; i) the 

number of spores a person can inhale, ii) the toxicity of mycotoxins on molar basis, iii) 

the maximum amount of mycotoxin per spore (Kelman BJ, et al. Int J Toxicol. 23:3-10, 

2004, Attachment “M“), iv) the half-life of mycotoxins in humans, and v) the no 

observed effect level (NOEL) for even the most potent mycotoxins (Hardin BD, et al. J. 

Toxicol. Environ. Health A. 72:585-98, 2009, Attachment “N”). Given all these factors, 

it is not tenable to propose toxicity resulting from inhalation of mold spores in the air 

found in the vehicle in question.

b. Irritant effects. Irritant effects from mold can result from inhalation of a very large 

concentration of mold particulates in the air wherein the spores essentially become 

nuisance dust. Levels in the millions of spores/m3 or more would be required for this 

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effect, levels far beyond anything found in the vehicle in question. Additionally, in high 

enough concentrations, mold derived volatile organic compounds (VOCs), e.g. gasses 

that smell and give rise to the musty odor associated with mold, can cause local irritant 

effects, usually of the wet membranes of the eye, nose and mouth. However, VOC 

irritant effects generally occur at levels hundreds to thousands of times higher than the 

odor threshold. Furthermore, even if the plaintiff had had some local irritant effects from 

VOCs, albeit there is no data to support that supposition, such effects would have been

transient by definition, and would have disappeared within a week or two of no longer 

being in the vehicle in question.

Assessment and opinion.

• It is my opinion that the generally accepted mechanisms for mold and/or mold byproduct

induced adverse health effects are not relevant to Ms. Beckemeyer’s medical issues. , 

i.e. her complaints are not even potentially related to the mechanisms of accepted mold 

adverse health effects other than possibly some mild upper airway allergy.

IIIB. Opinions about the medical significance of the environmental testing and potential 

exposures of Ms. Beckemeyer from the vehicle(s) in question.

Background: Ms. Beckemeyer had the vehicle in question, a 2014 Toyota RAV 4 limited

assigned to her from May 4, 2016 until September 30, 2016. During that time, she was living 

in Butler Co Ohio and working in Ohio, Kentucky, and parts of Indiana.

The relevant metric for potential human exposure to mold and mold byproducts and 

subsequent dose calculations is sampling of respirable air (Attachments “B”-“H”, “M” and 

“N”.) While testing for molds and their byproducts on surfaces in a vehicle or home or inside 

walls may have relevance to remediation efforts, there is no way to determine or even estimate 

the levels of human exposure from such sources and to attempt to do so is speculation and not 

generally accepted methodology for assessing human exposure. Additionally, the respirable air 

sampling must be in a relevant timeframe in terms of when the individuals were in the location 

being sampled. One cannot sample locations months or years after the individual was there 

and say what was present when the subject was there.

Mr. Porter’s report provides an excellent summary of the Ms. Beckemeyer’s history of vehicle 

use and an in depth analysis of the multitude of testing performed. He also discusses her 

residence and work locale and their potential for airborne exposures to molds and other 

materials. His report provides an excellent analysis of the relevance of testing for molds, 

bacteria and endotoxin and their potential exposures and health effects and I will not repeat 

that information here. 

In addition to Mr. Porter’s report, there is a 7.25.18 Ecostratum report regarding on testing of 

the vehicle in question on 7.9.18. There was only a single air sample taken. This nonviable 

mold spore air testing in the vehicles interior air showed 1300 spores/m3 dominated by 690 

basidiospores (mushroom spores), 480 ascospores, 27 Chaetomium and 53 Cladosporium 

and 7 Alternaria. No Fusarium or Epicoccum spores were detected. No outdoor control sample 

was taken. As noted in Mr. Porter’s report detailed report, these levels of are in fact low and 

generally less than seen many days outside in the locale where Ms. Beckemeyer lived and is 

living.

Assessment and Opinion

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It is my opinion that the only samples that are possibly relevant to potential adverse health 

effects for Ms. Beckemeyer are the respirable air samples from the vehicle in question. Those 

samples do not give evidence that the air in the vehicle would have represented any form of 

health hazard to Ms. Beckemeyer. 

It is my opinion that since the testing of vehicle was more than a year after Ms. Beckemeyer 

was in the vehicle, it is speculation to say what the levels were at the time she was using it.

It is my opinion that respirable air levels of mold spores below 6500 spores/m3 are considered 

“low” by the National Allergy Board and that is in terms of potential health effects for subjects 

allergic to the mold in question. Given that the airborne levels measured of mold spores in the 

vehicle in question for molds Ms. Beckemeyer may be allergic to, were in fact low and far 

below those found in normal outdoor air in many places throughout the USA, the air in her 

vehicle would not have represented any form of increased health hazard risk to her.

IIID. Alternative/fringe health care and pseudo-diagnosis of Chronic Inflammatory 

Response Syndrome, aka “CIRS; Dr. Scott McMahon and Dr. Richie Shoemaker:

Dr. Scott McMahon is a pediatrician who practices medicine in Roswell, New Mexico. He 

practiced pediatrics until 2009 when he met Dr. Richie Shoemaker and began to practice

under the title of the Whole World Healthcare, PC. Dr. McMahon states in his resume that he is 

“specializing in the diagnosis and treatment of Chronic Immune Response Syndrome.” Dr. 

McMahon advertises himself as “Certified in Shoemaker Protocol for the Treatment of Chronic 

Immune Response Syndrome”. Dr. McMahon appears to be proud of the fact he was the “First 

(Shoemaker) certified practitioner in the world” (McMahon Resume, page 1, March 2015), a 

very dubious distinction indeed given that Dr. Shoemaker and his diagnosis and management 

of his so-called Chronic Immune Response Syndrome are outside the widest bounds of 

generally accepted medicine as will be discussed below. Dr. McMahon has had no postgraduate formal education or training in immunology, clinical immunology, internal medicine, or 

pulmonary medicine. 

Dr. McMahon wrote a report dated 8.31.18 regarding Ms. Beckemeyer’s medical issues. Ms. 

Beckemeyer testified that he examined her in a hotel room in Indianapolis Indiana on 7.30.18. 

Dr. McMahon’s report says he also spoke with her on the phone on 7.24.18, and again on 

8.19.18.

D1. McMahon report is focused on his opinion that Ms. Beckemeyer has chronic 

inflammatory response syndrome (“CIRS”) and that CIRS is the only known illness that could 

cause all the symptoms that Ms. Beckemeyer reports. Dr. McMahon clearly believes that the 

overarching diagnosis for all Ms. Beckemeyer woes is CIRS. CIRS was invented by a former 

practicing family physician, Dr. Richie Shoemaker. Indeed, Ms. Beckemeyer has discussed 

her case with Dr. Shoemaker even though he is no longer licensed to practice medicine. The 

report from Dr. McMahon about Ms. Beckemeyer is simply a recitation of the ideas put forth by 

Dr. Shoemaker who has been marketing himself and his “patent pending” diagnosis of CIRS 

(United States Patent Application Publication, Pub. No.: US 2014/0046143 A1 Shoemaker et 

al., Pub. Date: Feb. 13, 2014, Methods For Diagnosing, Treating, And Monitoring Chronic 

Inflammatory Response Syndrome).

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As proposed by Dr. Shoemaker and regurgitated by Dr. McMahon, CIRS represents an 

sustained uncontrolled activation of the “innate immune system” resulting from indoor and 

remarkably only indoor exposure to any/all of a host of potential microbes/microbial products 

that results in a panoply of systemic and organ specific symptoms and signs. Additionally, they

proposes that exposure to such microbes/microbial products in the future will lead to enhanced 

exacerbations of the subjects’ CIRS. According to Drs. Shoemaker and McMahon, there is no 

detectable lower limit for an exposure that can induce CIRS.

Dr. Richie Shoemaker is a former family practice physician from Maryland who is a self-styled 

“mold expert”. He withdrew from the practice medicine in 2013 while under investigation by 

the Maryland Medical Board. Subsequently, the Maryland Medical Board issued a highly 

critical reprimand letter to Dr. Shoemaker. (Attachment “O”). The Medical Board’s decision was

“should the physician resume the practice of medicine the physician will be placed on probation for 

minimum of two years with terms and conditions. The board found the physician failed to meet the 

standard of care.” https://www.mbp.state.md.us/bpqapp/PProfile.asp. Subsequently, Dr. Shoemaker 

then began to market a program where for $3000; other physicians could be “certified” by Dr. 

Shoemaker in his protocol for diagnosis and treatment of “CIRS.” Thus, Dr. Shoemaker trained and 

“certified” Dr. McMahon.

D1a. Assessment and Opinions re CIRS:

• It is my opinion that Dr. Shoemaker invented the “illness” he and others like Dr. 

McMahon currently call Chronic Immune Response Syndrome or “CIRS.” This 

purported syndrome is not generally accepted entity in the medical community. CIRS is 

a diagnosis that is unique to Dr. Shoemaker and his followers such as Dr. McMahon. 

Dr. Shoemaker has applied various terms (e.g. Biotoxin illness, Building Related Illness, 

Wet Building Syndrome) and variable criteria to this purported illness over the past 10+ 

years. 

• It is my opinion that Dr. Shoemaker and Dr. McMahon’s allegation that CIRS is selfsustaining reaction of the innate immune system is in direct conflict with what is known 

about the human innate immune response.

• It is my opinion that many of the battery of tests Drs. McMahon and Shoemaker use to 

support their diagnosis of CIRS are not generally accepted methodology for any 

purpose in clinical medicine much less for the purpose for which he employs them. 

• It is my opinion that Drs. McMahon and Shoemaker fail to employ the proper tests to 

define if the type of condition he alleges CIRS represents, e.g. a systemic inflammatory 

response is actually present. 

• It is my opinion that the proposed treatment of CIRS with cholestyramine, Welchol, 

erythropoietin and pioglitazone is both inappropriate and, in the case of the latter two 

medications, dangerous. I will use this use of oral cholestyramine by way of example to 

demonstrate the lack of logical thought by CIRS practitioners. Oral cholestyramine can 

bind to lipophilic (lipid-liking) negatively charged substances such as cholesterol in the 

GI tract. Thus, it can be used to remove orally ingested negatively charged lipophilic 

toxins and/or toxins that recirculate via the liver and biliary system. However, the mold 

toxins CIRS advocates allege they are dealing with are not ingested but inhaled thus 

they are not in the GI tract nor are mycotoxins excreted/recirculate via the liver/biliary 

system. Furthermore, mycotoxins are not negatively charged molecules. Thus giving 

oral cholestyramine for alleged mycotoxin inhalation exposure is completely illogical. 

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Furthermore, the time mycotoxins remain in the body is generally less than a week so 

the later or long term use of oral cholestyramine, even if it was capable of removing 

mycotoxins (which it is not), as suggested by Drs. Shoemaker and adopted by Dr. 

McMahon is illogical. 

• It is my opinion that Dr. Shoemaker and Dr. McMahon’s proposal that immune 

responses in CIRS and in immunology in general fail to follow dose response 

relationships is profoundly mistaken and in direct contrast what is known about the 

immune system. All medicine including toxicology and immunology involve a dose 

response. For example, Dr. McMahon has alleged there is no dose response in 

anaphylaxis but that is completely mistaken. All of these events have a dose response 

even when there is an immune cascade that follows the triggering event. 

Immunologists clearly recognize the amplification fact of immune cascades but they are 

all dose dependent. Nothing Dr. McMahon, Dr. Shoemaker or others can say will alter 

the truth of the dose response in all of medical science as was first espoused by 

Paracelsus in the 15th Century.

• It is my opinion that the literature that Dr. Shoemaker and Dr. Mahon cite as actually 

supporting their opinions regarding CIRS has been generated by Dr. Shoemaker and 

his colleagues and true experts in the relevant fields do not generally accept that work 

as reliable. 

• It is my opinion that given the shortcomings of Dr. Shoemaker’s methodology, theories 

and diagnoses, it is not surprising that Dr. Shoemaker testimony has been excluded by 

the courts on at least 11 occasions as listed in Attachment “P” 

• It is my opinion that Dr. Shoemakers whole approach was soundly criticized by the 

Federal Bench in the Young matter (Attachment “Q”), a matter in which his testimony 

was excluded by the Court.

• It is my overarching opinion that Dr. McMahon, in diagnosing Ms. Beckemeyer with 

CIRS, is not practicing generally accepted medicine.

Dr. McMahon alleges that the 2008 General Accounting Office document entitled “Indoor 

Mold: Better Coordination of Research on Health Effects and More Consistent Guidance 

Would Improve Federal Efforts.” validates a set of diagnostic criteria for CIRS. 

• It is my opinion that Dr. McMahon’s statements that the GAO document validates a set 

of diagnostic criteria for CIRS is false. Nowhere in the entire GAO document does it 

mention CIRS or Dr. Shoemaker (or Dr. McMahon) and the document does not provide 

any form of validation of CIRS criteria. The document prepared by General Accounting 

Office of the Federal Government is not a scientific analysis of data. Its purpose was to 

analyze the research situation at a Federal level of effort. The GAO reviewed 20 written 

“reviews” and some government-generated documents. The conclusion of the 

document makes this agenda clear: “Better coordination of research on health efforts 

and more consistent guidance would improve federal efforts.” Clearly, the GAO 

document is not a scientific contribution but an analysis of governmental undertaking in 

the area of indoor mold. 

Dr. McMahon says that each of the lab tests he uses is approved by CLIA.

• It is my opinion that the statement by Dr. McMahon that each of the lab tests he uses is 

approved by CLIA is false. CLIA (the federal Clinical Laboratory Improvement Act) 

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simply is not involved at all in the “approval” of laboratory tests. Any expert in laboratory 

medicine also knows that even the FDA does not approve laboratory tests. The FDA 

clears test kits that are sold for diagnostic use in more than one state. In contrast, most

of the tests used by Dr. McMahon to make his diagnosis of CIRS are not FDA cleared

but are “home brew” tests developed by and using in an individual laboratory and thus 

are not subject to oversight by any governmental agency.

Dr. McMahon relies on the Dr. Shoemaker’s interpretation of HLA-Dr (a set immune 

response gene loci) of Ms. Beckemeyer to categorize her as susceptible to and having 

CIRS.

• It is my opinion that Dr. Shoemaker and McMahon’s purported HLA-Dr typing 

categorization as to susceptibility to mold related or other processes is completely

baseless and has no dipositive value.

Dr. McMahon, in his report, says that Ms. Beckemeyer’s NeuroQuant® test of 6.13.17 

shows an “increase in the forebrain parenchyma size and atrophy of the caudate nucleus 

and pallidum. Her mold scoring would be 4 of a possible 8 which is a positive result for 

structural brain damage caused by CIRS”.

Assessment and Opinion:

• It is my opinion that the NeuroQuant® test is not generally accepted as a valid measure 

of mold exposure or mold related CNS effects. The (mis)use of this test in making the 

pseudo-diagnosis of CIRS is another misadventure popularized by Dr. Richie 

Shoemaker much like his misuse of HLA-Dr typing. Parenthetically, the official results of 

Ms. Beckemeyer 6.13.17 NeuroQuant® test for accepted measurements show readings 

within the age-matched reference charts, e.g. a normal result.

• Notably, neither the Institute of Medicine nor the World Health Organization found 

evidence linking exposure to mold or dampness with any neurological adverse end 

points. (Attachments “B” and “D”). Dr. Paul Lees-Haley nicely summarized the issue 

of Mold Neurotoxicity in an article entitled Mold Neurotoxicity: Validity, Reliability and 

Baloney http://users.physics.harvard.edu/~wilson/soundscience/mold/lees.html.

Drs. McMahan alleges that Ms. Beckemeyer’s serum MSH level is low at 5 pg/mL Dr. 

McMahon alleges that her “low” MSH is part of CIRS. Dr. McMahan and Dr. Shoemaker 

claim that lower limit of the reference value for MSH is 35 pg/mL even though the 

Laboratory doing the tested reports a reference range of 0 (i.e., below the limit of detection)

to 100 pg/mL.

Assessment and Opinion:

• It is my opinion Ms. Beckemeyer’s serum MSH level is well within the true reference 

range as defined by the laboratory doing the test. 

• It is my opinion that Drs. McMahan and Shoemaker have arbitrarily defined their own 

“normal” values for serum MSH, and in doing so, ignore the reference values as 

defined by the laboratory doing the test. What Drs. McMahon and Shoemaker have 

done is far outside the bounds of generally accepted practice. While they allege that

the laboratory reference range of 0 (i.e., below the limit of detection) to 100 pg/mL 

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provided by the testing laboratory is wrong, they provide no real data to support their

belief that the lower limit of the reference value for MSH should be 35 pg/mL.

Dr. McMahon says that there no other single disease other than CIRS that could be responsible for all 

of Ms. Beckemeyer’s myriad of complaints. 

• It is my opinion that there is no single true pathophysiologic disease that encompasses all of 

Ms. Beckemeyer’s medical issues; Indeed, Ms. Beckemeyer has a number of distinct medical 

issues, each of which should be addressed individually. Such a set of different disease 

processes is typical for 60-year-old individuals. 

• It is my opinion that Dr. McMahon’s belief that CIRS can explain everything that troubles Ms. 

Beckemeyer (or anyone else) is based on the fact the hypothetical construct of CIRS has no 

boundaries. They use the rubric of CIRS such that it can be applied to any subject to explain

any set of issues, i.e. is all-inclusive and thus becomes meaningless as a specific disease 

process.

IIIE. Summary of Opinions.

• It is my overarching opinion that Ms. Beckemeyer’s medical complaints and 

issues past or present were or are not due to exposure to molds, bacteria or 

mold/bacteria byproducts that she may have experienced related to the vehicle in 

question.. 

• It is my overarching opinion that the environmental testing of respirable air in Ms. 

Beckemeyer’s vehicle does not give evidence that the level of mold spores 

indicate any form of increased health hazard to Ms. Beckemeyer. 

• It is my overarching opinion that Dr. Scott McMahon does not practice generally 

accepted medicine in making the pseudo-diagnosis of CIRS. In doing so, he 

follows the fatally flawed practices of Dr. Richie Shoemaker, a former family 

practice physician from Maryland who is a self-styled mold “expert” and who 

withdrew from the practice medicine when under investigation and about to be 

sanctioned by the Maryland Medical Board.

• The opinions expressed in this report are more probable than not.

• The opinions expressed in the report are based on the data available to me at the 

time of this writing. Should new data become available, I reserve the right to 

modify the opinions in this report based on that new information.

IV. PUBLICATIONS: 

All of my publications are listed in my CV/bibliography (Attachment “A”), are available in the 

public domain, and can be accessed via PubMed at https://www.ncbi.nlm.nih.gov/pubmed/ .

V. PRIOR TESTIMONY

A list of my testimony in the past four years is provided as Attachment “R”.

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VI. FEES

My compensation for preparation of this report is at a rate of $720/hour. My fees are $720/hour 

for consultation time and $900/hour for testimony time.

Respectfully submitted,

November 22, 2018

Andrew Saxon, MD Date

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