oxins 2013, 5, 605-617; doi:10.3390/toxins5040605

toxins

ISSN 2072-6651

www.mdpi.com/journal/toxins

Article

Detection of Mycotoxins in Patients with Chronic Fatigue

Syndrome

Joseph H. Brewer 1,*, Jack D. Thrasher 2, David C. Straus 3, Roberta A. Madison 4 and

Dennis Hooper 5

1. Plaza Infectious Disease and St. Luke’s Hospital, 4320 Wornall Road, Suite 440, Kansas City,

MO 64111, USA

2. Citrus Heights, CA 95610, USA; E-Mail: toxicologist1@msn.com

3. Department of Immunology and Molecular Microbiology, Texas Tech University Health Sciences

Center, Lubbock, TX 79430, USA; E-Mail: David.Straus@ttuhsc.edu

4. California State University, Northridge, CA 91330, USA;

E-Mail: vchsc001@csun.edu

5. RealTime Laboratories, Carrollton, TX 75010, USA; E-Mail: dhooper@realtimelab.com

* Author to whom correspondence should be addressed; E-Mail: jbrewer@plazamedicine.com;

Tel.: +1-816-531-1550, Fax: +1-816-531-8277.

Received: 18 March 2013; in revised form: 1 April 2013 / Accepted: 3 April 2013 /

Published: 11 April 2013

Abstract: Over the past 20 years, exposure to mycotoxin producing mold has been

recognized as a significant health risk. Scientific literature has demonstrated mycotoxins as

possible causes of human disease in water-damaged buildings (WDB). This study was

conducted to determine if selected mycotoxins could be identified in human urine from

patients suffering from chronic fatigue syndrome (CFS). Patients (n = 112) with a prior

diagnosis of CFS were evaluated for mold exposure and the presence of mycotoxins in

their urine. Urine was tested for aflatoxins (AT), ochratoxin A (OTA) and macrocyclic

trichothecenes (MT) using Enzyme Linked Immunosorbent Assays (ELISA). Urine

specimens from 104 of 112 patients (93%) were positive for at least one mycotoxin (one in

the equivocal range). Almost 30% of the cases had more than one mycotoxin present. OTA

was the most prevalent mycotoxin detected (83%) with MT as the next most common

(44%). Exposure histories indicated current and/or past exposure to WDB in over 90% of

cases. Environmental testing was performed in the WDB from a subset of these patients.

This testing revealed the presence of potentially mycotoxin producing mold species and

mycotoxins in the environment of the WDB. Prior testing in a healthy control population

OPEN ACCESS

Toxins 2013, 5 606

with no history of exposure to a WDB or moldy environment (n = 55) by the same

laboratory, utilizing the same methods, revealed no positive cases at the limits of detection.

Keywords: mycotoxin; mold exposure; chronic fatigue syndrome; Stachybotrys

1. Introduction

Chronic fatigue syndrome (CFS), also called myalgic encephalitis, has been widely studied over the

past 25 years. Numerous mechanisms and theories have been proposed to explain its pathophysiology,

epidemiology, clinical features and causation [1–4]. Possible causations include infections (particularly

by viruses), oxidative stress, immune aberrations and toxic exposures, among others. However, no

single etiology has been confirmed to fully explain this syndrome. In many circumstances, these

patients remain chronically ill despite varying attempts at treatment [1–4].

During the same time frame, there has been a growing body of scientific literature indicating that

mycotoxins and exposure to mycotoxin producing molds has become hazardous to the health of

occupants of water-damaged buildings (WDB) (homes, schools and places of business).

Water-damaged environments contain a complex mixture of biocontaminants produced by both mold,

Gram-negative and Gram-positive bacteria [5]. Secondary metabolites of molds and bacteria have been

identified in the dust, carpeting, wallpaper, heating, ventilation and air-conditioning (HVAC) systems

and respirable airborne particulates [6–16]. In addition, mycotoxins have been identified in clinical

isolates from corneal keratitis, aspergillosis and from body fluids and tissues of individuals exposed to

moldy environments [17–25]. Interestingly, patients with mycotoxin exposure in WDB frequently

have clinical features similar to CFS [5,26–29].

In this study, urine specimens were tested by ELISA-based assay to look for the presence of

mycotoxins in a group of patients with CFS. These results were compared to healthy control subjects

previously reported by the same testing laboratory. Additionally, in several cases, the WDB that were

the source of exposure were investigated for environmental mold and/or mycotoxins. A hypothesis of

possible mitochondrial damage in CFS is presented following review of the literature.

2. Materials and Methods

2.1. Patients

The study was conducted for 6 months from 1 February 2012 to 31 July 2012. Patients with chronic

illnesses, many of whom were previously diagnosed with CFS, were seen in a private practice (JHB)

which is a consultative outpatient infectious disease clinic in Kansas City, Missouri. Out of

approximately 300 patients with chronic illness that were seen for routine follow up clinic visit,

112 met the criteria for a diagnosis of CFS as outlined by Fikuda, et al. in 1994 [4]. These patients

were from diverse geographic areas in the United States however, the majority resided in Midwestern

states. The patient ages ranged from 15 to 72 years with 84 (75%) females and 38 (25%) males. The

duration of symptoms ranged from 2 to 36 years with an average duration of 7.8 years. The illness was

so severe that 76 (68%) of the patients were either unable to work, receiving disability or unable to

Toxins 2013, 5 607

attend school. A past history of mold allergy and/or chronic sinusitis was present in 50 (48%) of the

patients. These patients failed to respond to treatments and their CFS symptoms lingered.

Common symptoms in this patient population included fatigue, headache, flu-like symptoms,

cognitive complaints, myalgia, arthralgia, gastrointestinal problems and various neurologic symptoms.

Other previous diagnoses included fibromyalgia, Lyme disease, peripheral neuropathy, orthostatic

intolerance (including postural orthostatic tachycardia syndrome and neural-mediated hypotension),

migraine, chronic dermatitis, gastroparesis, chronic abdominal pain, irritable bowel syndrome,

interstitial cystitis, anxiety, depression, chemical sensitivity, vertigo, chronic sinusitis, gluten

intolerance, tremor, myoclonus and cognitive dysfunction.

Routine laboratory parameters including complete blood count and chemistry panels were usually

normal. Immune testing had been performed previously in most of these patients. The most common

abnormality was diminished natural killer cell (NK) function. Other immune abnormalities were

occasionally noted (e.g., hypogammaglobulinemia).

Since these chronic conditions have been reported to be associated with exposure to mold and

bacteria in WDB and previous studies have shown an association between CFS and sick building

syndrome (SBS), it was decided to carry out an environmental history and discuss urine mycotoxin

testing [28]. During these follow up visits, over 90% of the 112 patients confirmed exposure to a WDB

and frequently the presence of a moldy environments in the home, workplace or both.

2.2. Control Subjects

Healthy control patients with no known toxic mold exposures in water-damaged buildings were

previously reported [21]. These controls (n = 55) consisted of 28 males and 27 females, ages 18 to

72 years. These patients were also from diverse geographic areas and resided in various areas of the

United States. Urine specimens from these individuals were used to develop reference data for the

control group used in this study. Furthermore, the same control subjects were also asked about

complaints and/or symptoms related to mold exposure as documented in the peer reviewed literature at

the time of this study [30]. Symptoms that were screened included rhinitis, cough, headache,

respiratory symptoms, central nervous system symptoms, and fatigue. They did not give a history of

water-intrusion or mold growth in the workplace or at home. It was assumed that the controls had

exposure to foods and airborne mold spores that occur in their daily activity.

2.3. Mycotoxin Testing

Mycotoxin determination was conducted in similar fashion as described earlier with

modifications [21]. Competitive direct enzyme linked immunosorbant assays (ELISAs) were

conducted on all groups of mycotoxins studied (AT, OTA, MT). Validated, competitive direct ELISA

tests for MT and AT/OTA (private communication, RealTime Laboratories, Inc, Carrollton, TX) were

conducted on all urines submitted [21]. Validations have demonstrated that urine is the best fluid for

evaluation. However, the variability of urine matrix components such as organic compounds, pH and

electrolytes can affect antibody binding and assay performance in ELISA tests. To account for these

matrix effects, standard sample diluents for plasma serum, cell culture and other biological specimens

have been developed. No standard diluent has been developed for urine and many other biological

Toxins 2013, 5 608

fluids. Instead, phosphate buffered saline (PBS) was used as a “urine-like” diluent. In the validations

and continued testing of mycotoxins, a 10% methanol in PBS +10% methanol dilution (pH 7.2–7.4)

was used to compensate for the matrix effect in urine.

MT ELISA test: Urines were diluted at 1:5 to compensate for the matrix affect. Coated roridin A

(an MT) antibody ELISA wells (Beacon Analytic Inc., Maine) were inoculated with 100 microliters

(μL) of controls, calibrators, or patients specimens. One hundred microliters of diluted urine were

placed in each test well. One hundred μL of known MT (roridin A, Sigma Inc., St. Louis, MO)

calibrators (diluted: 10.0 μL/dL, 1.0 μL/dL, and 0.1 μL/dL, 0 μL/dL) and high, low, and negative

controls were placed in specific wells. Samples were incubated for 15 minutes at 21–25 degrees C

under continual rotation. One hundred μL of 1:1800 dilution of roridin A HRP-conjugate (Beacon

Analytic Inc., Maine) were added to each well and incubated for 15 minutes at 21–25 degrees C, under

continual mild rotation. All plates were washed 4 times with deionized water and tapped until

deionized water was removed. One hundred μL of substrate (Beacon Analytical Labs, Inc.) were

placed in each well and incubated 30 minutes at 21–25 degrees C under continual rotation. One

hundred μL of 1 N HCl were added to stop the reaction. The reactions were read on a Spectra Max 190

Spectrophotometer (Molecular Devices, Sunnyvale, CA) at 450 nm. Results were tabulated and

entered into a semilog software program (Beacon Analytical Labs, Inc.). Results were tabulated and

reported as ng/dL or parts per billion (ppb). All controls and calibrators met regulatory conditions as

specified in the standard operating procedures.

AT and OTA ELISA procedures: Urines were diluted at 1:7 to compensate for the matrix affect.

Coated wells (Neogen Corporation, Michigan) with either polyclonal antibodies to AT or OTA were

used in the separate mycotoxin procedures. Procedures for AT and OTA determinations were identical

except for the specific antibody coating the ELISA plates. Antibody ELISA wells (Neogen

Corporation) were inoculated with 100 μL of calibrators, controls or patients specimens. Initially,

100 μL of AT-HS conjugate (Neogen) and 100 μL of OTA conjugate (Neogen) were placed in the

respective antibody wells. One hundred μL of known antigen (AT or OTA, Trilogy Inc, MO)

calibrators for AT were 0, 1, 2, 4, and 8 ng/dL (ppb) and calibrators for OTA were 0, 2, 5, 10,

25 ng/dL (ppb). High, low, and negative controls for each mycotoxin were also placed in specific

wells. One hundred μL of diluted urine were placed in each test well. Plates were incubated at

21–25 degrees C for 10 minutes under continual mild rotation. All plates were washed 4 times with

deionized water and tapped until deionized water was removed. One hundred μL of substrate (Neogen)

were placed in each well and incubated 10 minutes at 21–25 degrees C under continual mild rotation.

One hundred 100 μL of 1N H2SO4 were added to stop the reaction. The reactions were read on a

Spectra Max 190 Spectrophotometer (Molecular Devices, Sunnyvale, CA) at 650 nm. Results were

tabulated and entered into a semilog software program (Neogen Inc). Results were tabulated and

reported as ng/dL or ppb. All controls and calibrators met regulatory conditions as specified in the

standard operating procedures.

2.4. Statistics

Statistics were performed on the patient data and controls for each of the three mycotoxins (AT,

OTA and MT). Two-sided independent t-tests were performed on OTA and the MT. Two-sided

Toxins 2013, 5 609

Fischer exact test was performed on the AT because the control data were negative (zero) for

this group.

3. Results and Discussion

Mycotoxin testing revealed the presence of at least one of the toxins in the urine of 104 out of 112

(93%) patients. This included 103 with positive results and one that was in the equivocal range for

OTA. The frequency of the various mycotoxins in the urine of CFS patients (based upon the suggested

detection limits of RealTime Laboratories) is summarized Table 1. OTA was most commonly detected

mycotoxin comprising 83% of the patients. This was followed by MT (44%) and AT (12%). The

presence of combinations of mycotoxins in the urine were follows: OTA + MT (23%), AT + MT (4%),

and all three (8%).

Table 1. This table summarizes the detection of the mycotoxins in the urine of chronic

fatigue syndrome (CFS) patients individually or in combinations. The ranges and averages

are based upon the actual number of individual positives for each mycotoxin.

Mycotoxin Positive (N, %) Range (ppb) Average (ppb)

ATa 13, 12% 1.1–9.4 4.67

OTAa 87, 83% 2–14.6 6.2

MTa 46, 44% 0.21–5.72 0.85

OTA + MT 24, 23% N/Ab N/Ab

AT + MT 4, 4% N/Ab N/Ab

AT, OTA, MT 8, 8% N/Ab N/Ab

a: Limits of Detection: AT (1 ppb); OTA (2.0 ppb); MT (0.2 ppb). b: N/A: Not applicable.

The CFS patients were compared to a previously published group of healthy control subjects that

had no history of exposure to a WDB or moldy environment. The frequency of detection of these three

mycotoxins in the CFS patients compared to controls is seen in Table 2.

Table 2. Detection of mycotoxins in CFS patients compared to healthy controls.

Patient Group Number Tested ATa,b OTAa,b MTa,b Any Mycotoxinb

CFS 112 12 (12%) 87 (83%) 46 (44%) 104 (93%)

Controlc 55 0 0 0 0

a: Limits of Detection: same as Table 1. b: Number positive, percent positive; c: Control group

previously published [21].

The concentration of mycotoxins in the urine of patients and controls were statistically analyzed to

determine if a difference existed between the two groups. These data are summarized in Table 3. The

concentrations were significantly elevated in the patients compared to controls as follows: AT

(0.43 ± 1.36 vs. 0 ± 0 ppb, p = 0.0007), OTA (5.26 ± 3.65 vs. 0.355 ± 0.457 ppb, p < 0.0001), and MT

(0.422 ± 0.714 vs. 0.0169 ± 0.0265 ppb, p < 0.001).

Toxins 2013, 5 610

Table 3. This table summarizes the independent two tailed t-tests performed on the

patients and controls with respect to ochratoxin A (OTA) and macrocyclic trichothecenes

(MT). The Fisher 2-Sided Exact test was performed on the aflatoxins (AT) because the

control group had non-detection of AT. The mean and standard deviations are listed in ppb

for each mycotoxin (patients and controls).

Mycotoxin Patients (N = 104)

(ppb)

Controls (N = 55)

(ppb)

t-value p

AT 0.43 ± 1.36 0 ± 0 —– 0.0007a

OTA 5.26 ± 3.65 0.355 ± 0.457 13.5 <0.0001

MT 0.422 ± 0.714 0.0169 ± 0.0265 5.78 <0.001

a: Fisher 2-Sided Exact Test Matrix: Controls (55 and 0); Patients (87 and 17).

Environmental histories of these patients were positive for exposure to WDB (many with visible

mold) in over 90% of the cases tested, including residential and/or workplace. In the residential group,

water damage to the basement was a common finding. However, other sources of water intrusion were

noted during history taking, which included water pipe leaks, roof leaks, window leaks and plugged

drains. In 24 patients, symptoms, which eventually became chronic, started within one year of the

exposure in the WDB.

Environmental tests (air spore counts, tape lifts and the examination of dust for mycotoxins) were

performed in 10 of the situations of the 104 patients (data not shown). In addition, two families

discussed below also conducted environmental testing. In the 10 cases mold genera associated with the

potential for mycotoxin production were found. In 8 of the situations, Stachybotrys was identified in

the WDB. In each of these 8 patients, MT was detected in the urine assay. In addition,

Aspergillus/Penicillium-like spores were detected in 8 buildings to which these patients were exposed.

The urine mycotoxin assays identified OTA in 5 patients and AT was present in 2 subjects.

Additionally, dust specimens collected from 5 homes and one office building were sent to RealTime

Laboratories for mycotoxin testing on environmental dust. MT was found in the dust samples from all

6 of these buildings. Small amounts of OTA were detected in 4 of the dust samples. There were

7 patients that had been exposed to mold in these buildings. Of these 7 patients, 6 had tested positive

for MT in the urine assay, with the levels ranging from 0.21 ppb to 5.72 ppb. Additionally, 4 of the

7 patients had tested positive for OTA with values ranging from 3.7 ppb to 10.2 ppb.

The two families that conducted environmental tests on their homes are presented below. The

families consisted of four individuals per household (Tables 4 and 5).

Family #1: The parents moved into a new home in 1991 and the family has lived there since. The

father began to develop symptoms of fatigue, muscle aches and cognitive problems, which was

subsequently diagnosed as CFS, within 4 months of moving into their new home. Within 3 years, the

mother developed CFS. Neither of the parents had any history to suggest occupational exposure

outside of the home. The two daughters were born and raised in that home. Both children developed

chronic illness (CFS) while living in the home. All four remain chronically ill (CFS). Urine AT, OTA

and MT concentrations (ppb) for each family member were as follows: father 0, 0, 0.59; mother 0, 3.6,

0.19; daughter 0, 4.2, 0.13 and another daughter 0, 3.6 and 0.17. Table 4 summarizes the results from

this family.

Toxins 2013, 5 611

Table 4. Detection of various mycotoxins in the urine of members of Family #1.

Family

member

Age Sex ATa

(ppb)

OTAa

(ppb)

MTa

(ppb)

Father 50 M 0 0 0.59

Mother 49 F 0 3.6 0.19

Child 19 F 0 4.2 0.13

Child 16 F 0 3.6 0.17

a: Limits of detection same as Table 1.

Standard air testing from their home revealed high numbers of Aspergillus spores in one area of the

home. Dust samples were collected on three different occasions from top of doorway jambs, kitchen

cabinets, bedroom, living room, kitchen, and home office and sent to Mycometrics LLC, (Monmouth

Junction NJ) for MSQPCR-36 (ERMI) testing [31]. The moldiness indices for these samples were

8.61, 16.54 and 16.7. Mycotoxin producing molds identified in dust samples were as follows:

Aspergillus (flavus, fumigatus, niger, ochraceus and versicolor); Penicillium (brevicompactum,

purpurogenum, crustosum, corylophilum and chrysogenum); Chaetomium globosum, Stachybotrys

chartarum and Trichoderma viride. A dust sample from under the refrigerator sent to RealTime

Laboratories for mycotoxin testing revealed MT (0.42 ppb) and OTA (0.6 ppb). The family had no

idea there was a “mold problem” in their home until 2012 when the environmental testing

was completed.

Family #2: All members of this family had chronic illness (CFS, celiac disease, chemical

hypersensitivity) which had developed after living in this home. The family moved into a home in

1997 and within months discovered problems with the exterior drainage which led to water intrusion.

There was subsequent flooding of the lower level of the home on multiple occasions. Environmental

air sampling of the home in 2005 revealed Aspergillus/Penicillium-like spores and

Stachybotrys-spores. The family moved to a different home in 2005 (within months of the testing

results) but all remained ill. The father had no history of occupational exposure outside the home and

the mother did not work outside the home during this time frame. The urine mycotoxin levels (ppb) for

AT, OTA, and MT in this family were as follows: father 0, 4.6, 0.02; mother 0, 6.8, 0.01; son 0.5, 6.1,

0.48 and daughter 0, 2.3, 0.03. The results for this family are seen in Table 5.

Table 5. Detection of various mycotoxins in the urine of members of Family #2.

Family

member

Age Sex ATa

(ppb)

OTAa

(ppb)

MTa

(ppb)

Father 49 M 0 4.6 0.02

Mother 54 F 0 6.8 0.01

Child 23 M 0.5 6.1 0.48

Child 15 F 0 2.3 0.03

a: Limits of detection same as Table 1.

The etiology of CFS has been studied for several decades and numerous proposed etiologies have

been suggested [1–4]. Studies of CFS patients have demonstrated evidence of increased viral

activation, oxidative stress, immune abnormalities, neurocognitive features and endocrine

abnormalities [1,2]. In addition, CFS patients have mitochondrial dysfunction with impaired oxidative

Toxins 2013, 5 612

phosphorylation, low ATP stores and increased lactic acid with exercise [32–34]. Individuals that have

been exposed to WDB frequently have clinical features similar to CFS [5,22–29]. One study reported

concurrent sick building syndrome and CFS [28]. However, it should be recognized that additional

symptoms in CFS patients include fibromyalgia, headaches, loss of balance, neurocognitive

difficulties, flu-like symptoms, irritable bowel syndrome, anxiety, depression, among others

symptoms.

In this study, patients with a prior diagnosis of CFS were evaluated for the presence of mycotoxins

utilizing a sensitive and specific ELISA-based urine assay for three common mycotoxins. Ninety-three

percent of the cases demonstrated the presence of at least one of the mycotoxins in the urine. Over

90% of the patients gave a history of exposure to WDB. Additionally, mycotoxin-producing mold

species, mycotoxins or both were demonstrated in WDB that were associated with exposures in 18 of

these patients. The demonstration of the actual toxins in dust samples from the buildings in which the

patients either lived or worked is of considerable interest. This is because the same mycotoxins were

recovered from the urine of these patients. Trichothecene mycotoxins can be found in small fragments

as well as in conidia [7]. Furthermore, a variety of mycotoxins and bacterial exotoxins are present in

the dust and building materials of WDB [8–16]. Therefore, exposure to microbial toxins is most likely

underestimated, particularly since mold and bacteria shed fine respirable particulates less than 1 micron

in diameter in water-damaged conditions that contain toxins and other by-products [5,6,35–40].

The common denominators in these patients included CFS, additional symptoms, a water-damaged

environment, indoor mold and urine specimens positive for mycotoxins. OTA was the most common

mycotoxin detected in 83% of subjects followed by MT (44%) and AT (13%). Interestingly, more than

one of the mycotoxins was also present ranging from 8% (all three mycotoxins) to 23% (MT and

OTA) (Table 1). Moreover, the major mycotoxin in the urine of the two families (Tables 4 and 5) was

OTA, while MT were positive in two of the subjects. The question that arises is what is the probable

role of these mycotoxins in the symptoms experienced by the patients in this study? The Mitochondrial

Disease Foundation lists several masquerader health problems that are associated with mitochondrial

deficiency, which include the following organs: central nervous system, heart, peripheral nerves,

muscles, liver, ears, eyes, pancreas, digestive system and endocrine system. Manifestations of

mitochondrial deficiency can include autoimmune disorders, chronic fatigue, neurodegenerative

disorders (amyotrophic lateral sclerosis, multiple sclerosis, Parkinson’s disease), depression, other

psychiatric disorders, glycogen storage disorders, among others [41].

In vivo and in vitro studies have demonstrated that mycotoxins cause mitochondrial dysfunction.

Aflatoxins alter mitochondria as follows: mitochondrial DNA adducts, inhibition of protein synthesis,

pleomorphism, disruption of cristae, membrane damage and induction of apoptosis [42–45].

Trichothecenes have multiple inhibitory effects that include oxidative stress, apoptosis, inhibition of

protein, RNA and DNA synthesis, opening of phosphorescent Pt(II)-coporporphyrin (PtCP) and loss of

transmembrane potential and mitochondrial translation [46–50]. With respect to OTA the primary

thrust has been detecting its role in urinary tract and kidney diseases. However, the research into

kidney diseases has shown that OTA is also a mitochondrial poison. Mitochondrial abnormalities

resulting from OTA include membrane swelling, disarray of cristae, loss of transmembrane potential,

inhibition of succinate cytochrome c reductase and succinate dehydrogenase and inhibition of

succinate-supported electron transfer, and activities of the respiratory chain. The toxicity of OTA

Toxins 2013, 5 613

appears to result from oxidative stress leading to nuclear DNA damage, cytotoxicity and

apoptosis [51–54]. Thus, it appears that mitochondrial dysfunction may be correlated with the presence

of CFS and other symptoms in these patients.

The patients presented in this study had multiple symptoms including those consistent with CFS as

reported by others [22–29,55,56]. They had increased concentrations of AT, OTA and MT in their

urine samples compared to a group of previously published healthy controls. Their health conditions

and symptoms in these patients were suggestive of mitochondrial dysfunction as reported in subjects

with CFS [32–34]. In addition, the symptom complex of these patients was suggestive of

mitochondrial disease as reported by the Mitochondrial Disease Foundation [41]. Moreover, AT, OTA

and MT can cause mitochondrial damage [42–54].

4. Conclusions

Mycotoxins can be detected in the urine in a very high percentage of patients with CFS. This is in

contrast to a prior study of a healthy, non-WDB exposed control population in which no mycotoxins

were found at the levels of detection. The majority of the CFS patients had prior exposure to WDB.

Environmental testing in a subset of these patients confirmed mold and mycotoxin exposure. We

present the hypothesis that mitochondrial dysfunction is a possible cause of the health problems of

these patients. The mitochondrial dysfunction may be triggered and accentuated by exposure

to mycotoxins.

Conflict of Interest

Dr. Brewer and Madison declare no conflict of interest. Drs. Straus, Hooper and Thrasher have

served as expert witnesses in mold and mycotoxin exposure litigation.

References

1.