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Toxic Mold and Mycotoxins in Neurotoxicity Cases: Stachybotrys, Fusarium, Trichoderma, Aspergillus, Penicillium, Cladosporium, Alternaria, Trichothecenes


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Presented is the argument that psychologists and neuropsychologists have no scientific basis for rendering opinions about causation given the current state of the literature. The critical question is whether in a residence or office inhalation of mold spores or mold metabolites, including mycotoxins, causes neuropsychological impairment or mental and emotional disorders. There has not been sufficient research to support such conclusions. Nonetheless, in the context of litigation, speculative opinions are rendered in lieu of scientifically well-founded conclusions. Resources for recognizing and coping with pseudoscientific arguments are suggested.
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Paul R. Lees-Haley, PhD, ABPP
Independent Practice
Health Education Services
2915 Bob Wallace Avenue
Huntsville, Alabama 35805
Address correspondence to:
Paul R. Lees-Haley, PhD, ABPP
3021 Panorama Drive
Huntsville, Alabama 35801
Paul R. Lees-Haley, PhD, ABPP, is in independent
practice in Huntsville, Alabama.
Acknowledgements: Portions of this article were present-
ed at the conference entitled “Mold Medicine and Mold
Science: Its Practical Applications for Patient Care, Reme-
diation and Claims” hosted by the International Center for
Toxicology and Medicine and the Georgetown University
Department of Pharmacology, May 13–14, 2002. The author
thanks Dan Sudakin, Ronald Gots, Christopher Williams,
Lue English, Elizabeth Fox, Deborah Anderson, and the five
unidentified peer reviewers for their valuable contributions
to the work that led to this article.
This article is reproduced with permission of the publisher
from: Lees-Haley, P.R., “Toxic mold and mycotoxins in neu-
rotoxicity cases: stachybotrys, fusarium, trichoderma,
aspergillus, penicillin, cladosporium, alternaria, tricho-
thecenes,” Psychological Reports, 2003, 93, 561–584.
Mold neurotoxicity is an increasingly common allegation
in personal injury litigation, although conspicuously absent
in customary clinical practice. Time magazine’s Anita
Hamilton, in her June 24, 2001 article “Beware: Toxic
Mold” warned readers that “Like some sort of biblical
plague, toxic mold has been creeping through homes,
schools and other buildings across the U.S.
She went on
to say, “The biggest winners are the industries feeding off
mold mania.
The current toxic mold controversy appears
to be driven more by lawyers, testers, and remediators than
by scientific disagreements. Alleged central nervous sys-
tem effects are variously referred to as brain damage, toxic
encephalopathy, cognitive deficits, neurobehavioral
deficits, neuropsychological impairment, and as facets of
sick building syndrome or environmental illness. The
symptoms we see in forensic cases include memory
deficits, difficulty concentrating, problems with language
and reasoning, mental fatigue, depression, anxiety, and
numerous others.
In some cases the plaintiffs allege
dozens of symptoms they attribute to mold exposure.
The primary problem with the allegations of psychological
and neuropsychological impairment due to mold inhalation
Toxic Mold and Mycotoxins in Neurotoxicity Cases:
Stachybotrys, Fusarium, Trichoderma, Aspergillus,
Penicillium, Cladosporium, Alternaria, Trichothecenes
Vol. 11, No. 2 May 2004
Toxic Mold and Mycotoxins in Neurotoxicity
Cases: Stachybotrys, Fusarium, Trichoderma,
Aspergillus, Penicillium, Cladosporium,
Alternaria, Trichothecenes
Paul R. Lees-Haley, PhD, ABPP 1
Primary Multiple Drug-Resistant Tuberculosis:
A Case Report
Kevin L. Trangle, MD, L. Fleming Fallon, Jr., 15
MD, DrPH, Adebowale Awosika-Olumo,
Case Notes
Thomas R. McLean, MD, JD, FACS, Esq. 20
jcmc0405 final.qxd 5/3/04 11:05 AM Page 1
is that speculation has been substituted for empirically
established scientific reasoning. Based on the absence of
research in the neuropsychology and psychology literature,
as of this writing, there is no scientific basis for the allega-
tion that breathing mold spores or mycotoxins or other
mold metabolites in household and commercial office set-
tings causes neuropsychological impairment. The psycho-
logical and neuropsychological effects of these exposures
have not been established. But experts are expressing opin-
ions about causation in forensic cases, saying they cannot
think of any reason that a person suing for millions of dol-
lars might make subjective complaints other than because
they inhaled mold, and that the scientific literature does not
disprove their speculative opinions. These are not scientif-
ic arguments; they are arguments based on false assump-
tions, e.g., (1) patient attributions can establish cause, and
(2) although causation has not been established scientifi-
cally, it can be proven in a specific case.
The complaints that plaintiffs have been making in toxic
mold cases are variable and nonspecific. They do not con-
stitute a syndrome or pattern of essentially identical com-
plaints from one case to the next. Neither do their
neuropsychological test scores fall into a consistent pat-
tern. There is no fingerprint test profile or pattern of com-
plaints generally recognized as hallmarks of mold neuro-
The psychological and neuropsychological literature is
devoid of research on psychological and neuropsychologi-
cal effects of inhalation of mold spores and mold metabo-
lites such as mycotoxins. Searches of the PsycINFO
database as recently as February 8, 2003, for mycotoxin,
mycotoxins, mycotoxicity, mycotoxicosis, mold and
metabol,* mold and cognit,* mold and neuropsych,* mold
and memory, mold and concentration, mold and attention,
mold and toxic,* mold and mental disorder, mold and
encephal,* fungi and toxic,* fungi and neuropsych,* fungi
and cogni,* fungi and memory, fungi and concentration,
fungi and attention, fungi and encephal,* and fungi and
mental disorder, revealed not one controlled study of
humans despite the current wave of claims seen in forensic
psychological and forensic neuropsychological settings.
These searches included journal articles, books, reports,
dissertations, and chapters from 1872 to 2003. Repeated
searches in April and June 2003 did not produce new find-
ings based on psychological or neuropsychological testing,
with one exception. In the spring of 2003, a publication
cited as a 2002 article by Baldo, Ahmad, and Ruff
cussed below) appeared on the databases.
The psychological and neuropsychological effects of
inhalation of mold spores and mold metabolites such as
mycotoxins in residential and office settings simply have
not been studied in the psychological and neuropsycholog-
ical literature sufficiently to offer a scientific basis for
opinions about their hypothetical effects. Other than the
article above and another brief exception mentioned below,
similar searches in the medical literature (Medline/
PubMed) that employs psychological and neuropsycholog-
ical testing have revealed no such studies.
The paper most often cited in forensic cases as evidence of
neuropsychological impairment due to mold neurotoxicity
is not a scientific study.
It was not peer reviewed in any
conventional sense and the methodology was fatally
flawed. The paper reports having evaluated persons
exposed to Stachybotrys atra but used no control group
and did not include a standardized test battery adminis-
tered to all the participants. Alternative toxic exposures
were not investigated, not even other mold exposures. The
neuropsychological test scores of the people studied were
notable for being normal, not impaired. Due to these and
other limitations the report is mostly uninterpretable and
does not constitute scientific evidence of mold neurotoxi-
city. Notwithstanding these problems, lawyers and a small
number of experts refer to these findings as evidence of
mold neurotoxicity, e.g., in the famous Texas case of
Melinda Ballard and Ronald Allison v. Farmers Insurance.
In another relevant study involving objective testing, as
distinct from subjective reports (a study that was published
in a peer-reviewed journal), the briefly mentioned finding
Journal of Controversial Medical Claims 2 Vol. 11, No. 2
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jcmc0405 final.qxd 5/3/04 11:05 AM Page 2
was that the persons exposed to mold performed better on
cognitive testing than the controls.
found an increase in self-reported neurobehavioral
symptoms in a case report of alleged mold-exposed individu-
als but cautioned readers that these individuals were aware of
reports of adverse health effects of toxigenic fungi prior to
relating their subjective complaints, which improved substan-
tially after leaving the building. Sudakin
reported that many of
the people in this study were making claims for compensation,
and described his paper as one that discussed the hypothetical
role of mycotoxins (not mold exposure) in the context of
behavioral effects, and he concluded that this was a hypothesis
with unknown applicability to humans. He also said his paper
did not suggest that mold exposure may result in central nerv-
ous system changes.
The recent paper by Baldo, Ahmad and Ruff
neuropsychological testing but was based on a cross-sec-
tional sample that was so small and diverse that this was a
case study reporting anecdotal information, not a con-
trolled study that might shed light on causation. The infor-
mation in the article is so general that it is not clear what
population is the focus of this study. The plaintiffs were not
exposed to the same fungi, or exposed for a similar dura-
tion, or exposed in any measured amounts, and no data
were presented to clarify which molds or mycotoxins were
the independent variables in this study. Given that every
human on earth is exposed to mold, and there are an esti-
mated 100,000 fungi with varying properties,
lack of fur-
ther clarification of the independent variable was a critical
omission. The neuropsychological test results were
implausible. The Baldo et al. article has too many limita-
tions to be used as a basis for opinions about effects of
mold on human neuropsychological functioning. Unfortu-
nately, despite qualifying their work as preliminary, the
authors both imply and state conclusions that are not sup-
ported by their study or by the literature they cite.
Because their methodologies lack objective evidence that
mold or mycotoxin inhalation has caused brain injury,
experts claiming to have found such injuries are relying
heavily on subjective reports of symptoms and on tests that
are affected by response biases associated with litigation
and hazard perception.
This approach to forming causa-
tion conclusions is problematic for a number of reasons
that will be discussed in more detail below. One key limi-
tation, as noted above, is that there is no known pattern that
constitutes a neuropsychological or psychological syn-
drome or diagnosable mental disorder associated with
mycotoxin inhalation or inhalation of mold spores.
Many experts in litigated cases are ignoring the growing
body of research showing that patients in litigation behave
differently from other persons in ways that directly affect
assessment of the patient’s condition. Artifacts associated
with litigation appear to be affecting neuropsychological
test results.
Plaintiffs often report their pre-injury history
in unusually benign terms, and discount alternative expla-
nations for their complaints, such as important stressors in
their lives.
They respond to neuropsychological tests
more frequently in an impaired range even when no one is
claiming they have brain damage—not their lawyers, their
doctors, or the plaintiffs themselves. For example, plain-
tiffs making mild brain injury claims often respond to psy-
chological tests in a more impaired way than persons with
documented severe brain injury. Again, the test results
appear to be contaminated by biases arising from litigation
rather than being a true reflection of the extent of injury.
There is growing evidence that attorneys and other advo-
cates associated with litigated claims influence the psy-
chological and neuropsychological evidence in ways that
cause misleading and erroneous results.
Finally, it is
becoming increasingly clear that the amount of effort the
patient makes during neuropsychological testing has a
greater impact on the test results than the degree of injury.
In summary, the influence of the claims context is such a
powerful confounding force that it must be considered in
the process of differential diagnosis and ruled out.
Genuinely troubled people are particularly susceptible to
these influences, at times to their detriment. For example,
individuals with somatoform characteristics and histrionic
personalities tend to be suggestible
and therefore vulner-
able to zealots and advocates who tell them they are brain-
damaged and permanently injured by their toxic
environment. Most of us more or less ignore, or notice and
discount common “symptoms of life” such as transient
aches and pains, fluctuating ability to concentrate, tempo-
rary fatigue, feeling stressed, or inability to recall various
sorts of information such as a word or name or where we
left something.
However, when an expert claims these are
symptoms of mold neurotoxicity, a suggestible person may
focus more attention on these experiences, become
alarmed, and become involved in a vicious cycle of overin-
terpreting mild symptoms, becoming anxious, developing
more symptoms caused by the anxiety, and becoming even
more alarmed, sometimes to the point of virtually obsess-
ing over the symptoms.
Adding medication, which many
plaintiffs take in connection with these symptoms, increas-
es the likelihood that medication side effects will further
complicate the clinical picture, for example, by interfering
with concentration, memory, energy level, etc.
It is an
easy next step for the patient to conclude that, because
these feelings are more noticeable and more frequent late-
ly, they must have been caused by mold exposure as has
been suggested to them.
Although most of us think of ourselves as not presently
suffering the effects of brain injury due to mold or any-
thing else, empirical investigations have repeatedly shown
that surprisingly high rates of brain injury symptoms such
as memory and concentration complaints and fatigue are
Vol. 11, No. 2 3 Journal of Controversial Medical Claims
jcmc0405 final.qxd 5/3/04 11:05 AM Page 3
normal in diverse populations such as adults in general,
students and medical patients.
Likewise, epidemiological
studies of prevalence of psychiatric symptoms show that
rates of psychiatric illness are common and “greater than
previously thought to be the case.
Thus, when someone
begins a search for “psychopathology” it is not hard to
find. Administration of diagnostic tests to a random or
non-complaining population detects false positives and
actual pathology that was not apparent prior to the testing,
so it is no surprise that testing a group of plaintiffs reveals
apparent injury whether or not there is any.
Normal peo-
ple produce scores in the impaired range on several tests in
a detailed neuropsychological test battery,
but some
experts ignore these base rates (“normal levels of abnor-
mality”) and overinterpret a few low scores as indicative of
toxic brain injury.
In ambiguous settings, psychological influences play an espe-
cially important role in human perception, so it is not surpris-
ing that they are important in controversial arguments over
what is known about mold neurotoxicity. The information dis-
seminated by media, politicians, activists, litigating parties,
experts, and attorneys may cause important emotional reac-
tions in susceptible people. A claim may be false but it can
cause true alarm and genuine emotional distress if misleading
allegations are taken seriously.
It is critically important to use good science rather than
advocacy in the evaluation of mold neurotoxicity. Lawyers
and clinicians who cannot wait for facts (or actively reject
them) are relying largely on propaganda and social influ-
ence techniques such as those described by Cialdini
Pratkanis and Aronson.
For example, they use social
proof, repeated affirmations, appeals to authority, and
vividness to persuade people that baseless views are true.
Social proof is the tendency to believe what other people
believe. If an advocate creates the impression that other
people have concluded that mold caused them brain dam-
age, there is a natural tendency to agree and a subtle impli-
cation that one who disagrees lacks credibility.
Identifying a few people who believe a proposition and
encouraging them to go public (especially repeatedly) cre-
ates the impression that numerous people are discovering
something real.
For example, celebrities are called upon
to join in public outcries against perceived toxic exposures.
Repeated affirmations—literally, saying your claim over
and over again—creates the impression that the assertion is
true. After all, as everyone knows, where there is smoke,
there must be dry ice. Appeals to authority add weight to
these persuasions; if one or more of the people affirming a
belief is authoritative, e.g., a civic leader or expert, more
people will be persuaded. Sometimes politicians are per-
suaded to join in unfounded but politically popular rheto-
ric, e.g., when the US Congress condemned the American
Psychological Association based upon the mistaken belief
that research published by the APA was endorsing child
If we like the source of an opinion, we are more
likely to believe what is said. Thus, if a popular actor,
media figure, politician or local hero joins the process,
more of us will endorse the perceived reality.
In mold litigation, household names such as Ed McMahon and
Erin Brockovich have appeared in the national news related to
the toxic mold controversy. Vivid examples—especially dra-
matic, anecdotal case histories—often influence judgments
more than dull but more accurate quantitative examples. Pre-
senting a dramatic, close-up picture of frightening black mold
(Stachybotrys) may generate the feeling in the observer that
“this is bad” and permit a scientifically unfounded emotional
segue to the conclusion that anything that looks this bad must
cause the alleged harm.
A closely related problem is recent research showing how
false memories can be implanted or developed even when
there is no reason to suspect the individual of any intent to
deceive. For example, Elizabeth Loftus and her colleagues
have dramatically demonstrated the potential for introduc-
ing erroneous memories in interviews.
Such false memo-
ries are not necessarily subtle shades of gray; some are
dramatic and blatantly inaccurate recollections of events
that never happened.
Patients pursuing litigation report more intense, frequent, and
persistent symptoms than do non-litigating patients. For exam-
ple, a number of prospective studies have found that non-liti-
gating individuals with mild brain injury typically recover from
their symptoms within a few months of injury.
recovery of patients in litigation often defies expectations.
Their complaints, including memory loss, headache, dizziness,
concentration difficulty, blurred vision, photophobia, ringing
in the ears, irritability, fatigue, anxiety, and depression
reported to continue long after such symptoms normally
Numerous empirical investigations have documented
discrepancies between patients seeking compensation and
patients not seeking compensation.
Fee and Rutherford
pared the frequency of reported symptoms among patients with
mild brain injury who were in litigation with symptoms of oth-
ers not in litigation. After normalizing for severity of initial
injury, reporting rates were assessed for various symptoms
including headache, anxiety, irritability, dizziness, depression,
and insomnia. Litigating patients reported nearly twice as
many symptoms as non-litigating patients.
The discrepant nature of self-reported symptoms in com-
pensation seekers has been established with respect to psy-
chological as well as neuropsychological injuries.
Compensation-seeking patients have been found to report
more persistent psychological symptoms than patients with
Journal of Controversial Medical Claims 4 Vol. 11, No. 2
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similar injuries not seeking compensation. Frueh, Smith,
and Barker
for example, found that combat veterans seek-
ing service-connected disability for posttraumatic stress
disorder (PTSD) had significantly more pathological
scores on a wide range of psychological inventories and on
MMPI-2 validity indices than did combat veterans with
equivalent PTSD diagnoses not seeking compensation.
Pope, Butcher, and Seelen
noted that MMPI profiles of
patients with pending disability evaluations exhibit more
exaggeration and pathology. Their research also indicated
that genuinely disabled people not awaiting a disability
determination tend to produce MMPI profiles with normal
scale scores. Compensation seeking has been cited as one
of the most serious obstacles to successful treatment of
PTSD within the VA system.
Campbell and Tueth
reported that the system of compensation payments creates
a disincentive for recovery and noted that, “Rewarding
individuals for pain and disability, particularly on a long-
term basis, can have numerous negative consequences, and
ultimately may be a disservice to the patient.
Gold, and de Arellano
similarly identified compensation
as a confounder in cases of PTSD.
Health care providers have noted fundamental differences
between litigating and non-litigating patients, and “have
become increasingly suspicious of the genuineness of symp-
toms exhibited by plaintiffs because of the large disparity often
found between subjective complaints and objective findings.
Compared with non-litigating patients, patients seeking finan-
cial compensation may find treatment withheld because plain-
tiffs are perceived as resistant and noncompliant with
psychotherapeutic and rehabilitative services. When incentives
such as settlements may outweigh incentives such as getting
better, there may be noncompliance with helpful therapy and
searches for claim-supporting tests and care.
Not only do litigating patients report current symptoms at
higher rates and as persisting longer than do non-litigating
patients, but litigating patients tend to recall pre-injury
psychological and neuropsychological functioning as
superior to controls.
For example, Lees-Haley, et al.
asked litigating and non-litigating patients to recall how
problematic specific symptoms, behaviors, and aspects of
life were in the past. Compared to non-litigants, patients
seeking compensation recalled pre-injury functioning as
less problematic. These recalled variables, all relevant to
evaluations of “toxic mold” plaintiffs, included concentra-
tion, memory, fatigue, depression, anxiety, ability to attend
school or work, irritability, headache, confusion, self-
esteem, marriage, and relationships with children. Because
the apparent severity of injury depends upon a comparison
of pre- and post-injury functioning, this apparent worsen-
ing from pre- to post-injury bolsters the claim for compen-
sation. Therefore, by failing to take into account the
tendency of plaintiffs to overestimate their pre-injury sta-
tus, forensic examiners and triers of fact may overestimate
the severity of the injury.
It is important for examiners to recognize that these ten-
dencies are trends, not absolutes. They are group differ-
ences analogous to characteristics of a diagnostic group,
e.g., persons diagnosed as suffering from depression. It is
a mistake to presume that being a claimant or seeking com-
pensation is automatically equivalent to being a malinger-
er. The majority of plaintiffs do not appear to be
malingering. The problem of assessing claimants is analo-
gous to problems with interpreting data from job appli-
cants and persons examined by psychologists while
seeking to win custody of their children. We know from
years of experience that job applicants and individuals
seeking custody of their children have a distinct tendency
to present themselves in a favorable light during psycho-
logical evaluations.
Similarly, claimants show a bias in
the other direction, tending to emphasize ways of describ-
ing themselves that are consistent with their claims of
injury or disability.
Malingering is defined as the intentional production of
false or grossly exaggerated physical or psychological
symptoms motivated by external incentives such as finan-
cial gain, seeking drugs, avoiding work, evading criminal
prosecution, etc.
Contrary to what many of us used to
believe based on our clinical treatment experience, empir-
ical studies are finding that malingering is a common phe-
nomenon in forensic matters. The courts perhaps were
wiser than clinicians—they have long recognized this phe-
nomenon. References to the problem of fraudulent claims
and false testimony recur in published cases and legal com-
mentary throughout the history of law. The oldest known
code of laws, the Code of Hammurabi, addressed this
issue. (Hammurabi’s policy was to slay witnesses who tes-
tified falsely).
Indeed, the problem of false testimony is
the first issue addressed with every witness in every court
in every case: “Do you swear to tell the truth, the whole
truth, and nothing but the truth, so help you God?”
Patients seeking compensation have more incentive to produce
false or exaggerated symptoms than patients seeking treatment.
Over the years, estimates of the proportion of plaintiffs feign-
ing psychological deficits ranged from a low of 1 percent
over 50 percent.
In personal injury cases, feigned cognitive
deficits have been estimated at 64 percent
with 47 percent of
workers’ compensation possibly involving malingering.
Another study estimated the percentage of invalid memory
deficits in patients claiming persisting postconcussive syn-
drome as being between 33 percent and 60 percent.
by Binder
indicated that 33 percent of mild brain-injured sub-
jects seeking compensation malingered deficits on psychome-
tric testing. Such studies are relevant because the complaints
made by persistent postconcussive plaintiffs are remarkably
similar to those of many “toxic mold” plaintiffs. Both often
appear to be exhibiting response biases related to litigation.
Mittenberg, Patton, Canyock, & Condit
studied 33,531 cases
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involved in personal injury, disability, criminal or medical mat-
ters and found that 29 percent of personal injury, 30 percent of
disability, 19 percent of criminal, and 8 percent of medical
cases involved probable malingering and symptom exaggera-
tion. Mittenberg et al. found that 39 percent of mild head
injury, 35 percent of fibromyalgia/chronic fatigue, 31 percent
of chronic pain, 27 percent of neurotoxic, and 22 percent of
electrical injury claims resulted in diagnostic impressions of
probable malingering. In their study, diagnosis was supported
by multiple sources of evidence. Forensic examiners should
consider and rule out the possibility that symptom reports and
test results are the product of inaccurate presentation by plain-
tiffs during interviews and exaggeration of symptoms through
self-report inventories or tests. It has become the standard of
care to consider the possibility of malingering when perform-
ing a differential diagnosis in forensic cases.
Some psychologists and psychiatrists claim that plaintiffs
are unable to malinger mental disorders or neuropsycho-
logical deficits without detection by psychological experts.
However, there is substantial contrary empirical support.
Naïve individuals can fake psychological and neuropsy-
chological symptoms successfully when provided minimal
information about disorders.
In one investigation, partici-
pants asked to fake brain injury were provided detailed
information on the type of validity scales on the MMPI-2
and were given information on how to avoid getting
caught. This information enabled subjects to produce clin-
ically elevated profiles without significantly elevated
validity scales.
Uncoached individuals may report symptoms similar to
those of genuine patients on certain kinds of inventories,
such as symptom checklists.
Research indicates that
untrained individuals are able to endorse accurately symp-
toms and experiences of post-concussion syndrome,
well as major depression, generalized anxiety disorder, and
That naïve individuals can simulate psychopathol-
ogy without raising suspicion of malingering is problemat-
ic for expert evaluators. Information about some
psychological and neuropsychological disorders is readily
accessible to plaintiffs motivated to deceive. Berry
out that “Fabricators may become familiar with psychiatric
symptoms through personal acquaintances, perusal of vol-
umes such as the DSM-IV,
textbooks in psychiatry, or
even through exposure to lay sources such as magazine
articles and movies about individuals with mental disor-
Bury and Bagby note that a claimant motivated to
do so “can easily learn what symptoms must be reported to
qualify for the diagnosis” of PTSD.
The Internet provides
a wealth of information about mental disorders and neu-
ropsychological tests.
Many plaintiffs perform Internet searches that produce
claims and opinions of wildly varying reliability and valid-
ity. Although certain Web sites are a great aid to legitimate
research, innocent but suggestible persons may accept mis-
information, hyperbole, and speculation as fact. Attorneys,
clinicians, and various other interested parties are posting
a plethora of information on the Web. On March 18, 2002,
I entered “toxic mold” on and found 63,400
hits. At the top of all the 63,400 hits was the headline,
“Learn about the side effects of toxic mold!” The text
beneath this headline was not a referral to a scientist or
physician or toxicologist. Rather, there was a hypertext
referral to, which led immedi-
ately to, a site intro-
duced with the line “Toxic Mold info and access to
attorneys who specialize in Mold litigation.” On January
26, 2003, and June 16, 2003, I repeated the search for
“toxic mold” and found 115,000 and 138,000 hits, respec-
tively, on Google. A site laced with legal information, with
no readily identifiable responsible party, continued to head
the lists. The dramatic increase in Web postings on toxic
mold is a sign of the remarkable growth of interest, infor-
mation, and misinformation about the topic.
At a variety of information was
presented but at the top center of the Web page there was news
about someone suing for $65 million. This is not unique. Scan-
ning another Web site called “Toxic Mold and Tort News
Online Safety, Prevention, and Information” at http://www. we found the following introductory
statement: “The Toxic Mold Website is a comprehensive guide
to information regarding mold, toxic mold, safety, and preven-
tion. Our site also provides important legal rights and informa-
tion for those who have been adversely affected by Toxic Mold
in their home, workplace, and elsewhere.After a couple of
introductory paragraphs about “potentially fatal dangers” and
legal rights, there were four paragraphs of news, all four of
which were about how much money people had collected in
mold cases.
At The Mold Source at
starter.html there was a list of medical-legal experts about
whom the following claim was stated: “The following pro-
fessionals have established themselves, through their dedi-
cation, commitment and their overwhelming concern for
mankind, as the experts. They are the best the world has to
offer ‘us’, the fungi contaminated. Collectively, they retain
the majority of all known knowledge on fungi and fungal
poisoning related illnesses. . . . ” My point is not to ques-
tion the sincerity or integrity of the unidentified author of
these views. It is to illustrate the intensity of apparent
belief that we see in this issue and how this belief anoints
“toxic mold” experts.
The Toxic Mold Survivors Information and Support Group
at provides a
warning at the top of their home page about potential
adverse health effects of molds (including Stachybotrys,
Aspergillus & Penicillium, beneath the headline “Poisoned
by Toxic Molds?”). This site tells us that potential adverse
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health effects include “neurotoxic:-toxic encephalopathy”
[sic], memory and verbal problems, fatigue, malaise, verti-
go, dizziness, and depression. Although ostensibly a Web
site for a support group, litigation appears to be a major
interest of these “survivors.” For example, the home page
provides links to “Litigation” and “Next Asbestos?” (an
article entitled “Toxic mold . . . The Next Asbestos?” by
Sylvia Hsieh of Lawyers Weekly USA), plus links to the
websites of lawyers and expert witnesses who testify in
toxic tort litigation.
Background information from the medical literature and
relevant government agencies highlights the shaky founda-
tion for psychological and neuropsychological experts tes-
tifying that mold or mycotoxin inhalation causes
identifiable cognitive deficits. The following series of
opinions and findings by medical experts should inspire
some caution among psychological and neuropsychologi-
cal experts.
Medical experts indicate that fungi can cause human dis-
ease in four ways: allergy, mycosis (fungal infection), irri-
tation, and mycotoxicosis (poisoning by ingestion of a
Although it is known that many molds can
cause toxicity if ingested at high levels, at present, there is
no clear association of cause and effect between residential
and office airborne (inhaled) mold exposure and illness.
There have been no toxicologic and epidemiologic studies
of humans with adequate scientific or statistical power to
reach such conclusions.
Most of the reported studies in
the medical literature have been based on case studies or
small samples, and most have flawed methodology. A num-
ber of authors have noted that we have not yet clearly deter-
mined what fungi or mycotoxin may produce illness or
what dose is required.
Many studies have used self-report
measures of symptomatology and they have failed to rule
out or control for alternative causation, including whether
patients were involved in litigation.
Fung, et al.
point out
that immunological laboratory studies are non-specific,
which is ignored in some studies. The lack of symptom
specificity is problematic, since complaints such as
“chronic laryngitis, sinusitis, bronchitis, asthma, allergy,
and toxic encephalopathy have numerous etiologies.
According to the American College of Occupational and
Environmental Medicine (ACOEM) Evidence-based State-
ment, prepared under the auspices of the Council on Sci-
entific Affairs, peer-reviewed by the committee and
council and approved by the ACOEM Board of Directors
on October 27, 2002, “Current scientific evidence does not
support the proposition that human health has been
adversely affected by inhaled mycotoxins in home, school,
or office environments.
In their review of the relevant literature, investigators from
the National Institute for Occupational Safety and Health
at the Centers for Disease Control and Prevention (CDC
NIOSH) concluded that “This review of the literature indi-
cates that there is inadequate evidence to support the con-
clusion that exposure to mycotoxins in the indoor
(nonindustrial) environment is causally related to symp-
toms or illness among building occupants.
They also
concluded, “To support hypotheses regarding potential
adverse health consequences of mycotoxin exposure in the
nonindustrial environment, objective measures of adverse
health effects must be associated with some measure of
mycotoxin exposure, and comparisons must be made with
appropriate control populations; to date, such evidence has
not been forthcoming.
In another review of the literature, Robbins, Swenson,
Nealley, Gots, & Kelman
concluded, “Health-based
exposure standards for molds and mycotoxins do not yet
exist. While there is general agreement that active mold
growth in indoor environments is unsanitary and must be
corrected, the point at which mold contamination becomes
a threat to health is unknown.
Robbins and her col-
leagues wrote that “ . . . the current literature does not pro-
vide compelling evidence that exposure at levels expected
in most mold-contaminated indoor environments is likely
to result in measurable health effects.
Robbins, et al.
also noted, “Whether molds such as Stachybotrys should
be treated differently than other molds, when considering
cleanup or sampling and exposures issues, is also a con-
troversial subject.
In his review of the literature concerning Stachybotrys,
allergist Abba Terr concluded, “The current public concern
for adverse health effects from inhalation of Stachybotrys
spores in water-damaged buildings is not supported by
published reports in the medical literature.
According to Harriet Burge of the Harvard School of Pub-
lic Health, “People have become concerned about the
health effects of mycotoxins out of proportion to currently
estimated risk”
and “The fact that a mold is growing in a
home is not good evidence for exposure of any kind, and
certainly not evidence of danger.
Burge went on to say,
“In general, then, one can reassure patients that the symp-
toms they are experiencing, although real, are probably not
associated with mycotoxin exposure.
In May 2000, the American Industrial Hygiene Association
convened a forum to summarize findings of a panel of sci-
entists who had been assigned the task of evaluating the
scientific literature suggesting causal associations between
indoor exposure to mycotoxic fungi and adverse health
effects. This review panel included experts in pediatric pul-
monology, occupational health, epidemiology, microbiolo-
gy, toxicology, and industrial hygiene. “Ultimately, the
panel concluded that at this time there is not enough evi-
dence to support an association between mycotoxic fungi
and a change in the spectrum of illness, the severity of ill-
ness or an increase in risk of illness.
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Kuhn and Ghannoum
conducted a detailed review of
indoor mold and toxigenic fungi, emphasizing, but not lim-
iting their discussion to, Stachybotrys chartarum (atra).
They examined relevant case reports and studies and con-
cluded, “In summary, despite many reported subjective
complaints, there is no objective evidence for neurological
compromise caused by indoor mold exposure, in particular
from S. chartarum.
They also concluded, “. . .we have
not found supportive evidence for serious illness due to
Stachybotrys exposure in the contemporary environment.
Our conclusion is supported by several other recent
reports. . . .
In a review of current knowledge of Stachybotrys Char-
tarum (the most notorious mold in the litigation setting,
which is where most mold complaints are found), Dan
Sudakin, medical toxicologist, of the VA Medical Center in
Portland, Oregon, stated, “Although the hazards associated
with exposure to some mycotoxins have been well studied,
the health risks from environmental exposure to Stachy-
botrys remain poorly defined.
In a related conclusion,
Sudakin also stated, “Despite the far-reaching public health
measures that have emerged as a result of recent publica-
tions, the health risks from environmental exposure to
Stachybotrys remain poorly defined. The most current
research is limited by indirect assessment of exposure,
weak and inconsistent associations between exposure and
disease, and inadequate assessment of known confounders.
What is becoming clear is that
Stachybotrys and other
potentially toxigenic fungi are more common in the indoor
environment than has been previously acknowledged.
Janet Weiss, medical toxicologist at the University of Cal-
ifornia, San Francisco, wrote, “Although several outbreaks
of illness in humans have been attributed to respiratory
exposure to [Stachybotrys chartarum], the causal link
between fungal contamination in the indoor environment
and adverse health consequences has yet to be estab-
She further stated, “Data linking exposure with
health effects are unavailable for spore concentrations
found in typical indoor air environments.
Regarding the
emotional distress generated by clinicians who tell patients
that such exposures may cause cancer, one should note that
Weiss also stated, “There is no animal or epidemiological
evidence to indicate that S. chartarum is a carcinogen, yet
the popular press continues to raise this threat as if it were
a proven fact.
Fung, et al.
summarized the results of published studies
and reports regarding Stachybotrys mycotoxins related to
human toxicology and concluded, “Recently, airborne
mycotoxins associated with water-damaged buildings have
attracted the attention of health care professionals and the
public. The controversy over airborne Stachybotrys myco-
toxins originated from the extrapolation of data based on
case series without specific medical diagnoses. Some
reports imply a causal relationship between the presence of
Stachybotrys and poisoning. However, to demonstrate a
causal relationship between an environmental toxin and its
effects, several well-designed epidemiological studies with
sufficient statistical power are necessary.
These studies
have not yet been performed.
Based on their review of literature related to the microbi-
ology of mycotoxin-producing molds and their potential
role in human immunopathology in wet buildings,
Assoulin-Dayan, Leong, Shoenfeld, and Gershwin con-
cluded, “There has been increasing public attention to the
potential health risks of mold exposure, particularly in wet
buildings. A variety of molds has been isolated from both
damaged homes and businesses, including agents that
secrete toxigenic materials. One area that is attracting par-
ticular notice is the relative toxigenic potential of myco-
toxins. Although exposure to molds can produce
significant mucosal irritation, there are very few data to
suggest long-term ill effects. More importantly, there is no
evidence in humans that mold exposure leads to nonmu-
cosal pathology. In fact, many of the data on toxigenic
molds are derived from animal toxicity studies, and these
are based primarily, on ingestion. Although every attempt
should be made to improve the quality of indoor air,
including avoidance of molds, the human illnesses attrib-
uted to fungal exposure are, with the exception of invasive
infections and mold allergy, relatively rare.
Based on their review of all English language studies on
indoor mold exposure from 1966 to 2002, Fung and Hugh-
son concluded, “specific toxicity due to inhaled fungal tox-
ins has not been scientifically established”
They also
concluded, “Specific toxicity due to inhaled mycotoxins is
not well documented, and remains controversial.
In another review of the medical literature related to clinical
implications of mycotoxins and stachybotrys, Kaplan, Palmer
and Revankar wrote, “There has been considerable interest and
concern in recent years regarding the potential health effects of
mycotoxins in the indoor environment. Although the existence
of mycotoxins has been known for several decades, relatively
little is known about their effects in humans. What is known
comes almost exclusively from studies of ingestion as the route
of exposure. This review summarizes what is known regarding
health effects of mycotoxins in general and specifically exam-
ines the evidence for the role of indoor exposure to the fungi of
the genus Stachybotrys as a cause of disease in humans. Much
work remains to be done in the area of mycotoxin research. The
risk of health effects from ingestion seems much more wide-
spread than from indoor airborne exposure, although the latter
has received considerably more media attention. Rigorously
controlled studies are needed to clarify these issues.
The Texas Medical Association issued a report on “Black
Mold and Human Illness” that addressed Stachybotrys
They first noted that public attention to
Stachybotrys has increased, stating, “In Texas, this atten-
tion has been manifest not in scientific or medical publica-
tions, but rather in the lay press and in an increasing
number of insurance claims filed for mold remediation of
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homes and workplaces.
The Texas Medical Associa-
tion’s Council on Scientific Affairs was asked to update the
“state of the medical science” concerning Stachybotrys.
After performing their review, they reported their method
and conclusions: “To study this issue, the council conduct-
ed a search of medical and scientific literature and con-
tacted Texas and national experts/specialists. After
reviewing available data, the council has concluded that
public concern for adverse health effects from inhalation of
Stachybotrys spores in water-damaged buildings is gener-
ally not supported by published reports in medical litera-
Toxicologist Ronald Gots, in his conference paper entitled
“Correcting Mold Misinformation,” wrote, “Mold toxins at
indoor levels have never been shown scientifically to cause
any illness. Physicians generally do not accept that there is
any causal connection between them” and “Indoor expo-
sure to mold or mold toxins has never been proven to cause
brain damage.” He also added, “It is highly unlikely that
there is a home in the world without some Stachybotrys
spores in it.
reviewed literature on trichothecenes as related
to human health. He concluded, “Toxigenic fungi capable
of producing trichothecenes can be found in indoor and
outdoor environments throughout the world. . . . While the
effects of trichothecenes have been extensively studied in
animals the toxicology of these important mycotoxins
remains largely unexplored in humans. . . . More recent
reports suggesting human health risks from non-dietary
routes of exposure are difficult to objectively interpret, as
the assessment of hazard and exposure in these epidemio-
logical studies has primarily focused on toxigenic fungi,
not trichothecenes.
The Committee on Environmental Health of the American
Academy of Pediatrics wrote, “Pediatricians should be
aware that there is currently no method to test humans for
toxigenic molds such as Stachybotrys or mycotoxins.
The Centers for Disease Control and Prevention (CDC)
posts mold-related information for the public on their Web
site in the National Environmental Health section. In their
posting entitled “Questions and Answers on Stachybotrys
chartarum and other molds” they pose a series of questions
and answers.
Following are two of those questions and
the CDC answers:
Question: “I heard about toxic molds that grow in
homes and other buildings. Should I be concerned
about a serious health risk to me and my family?”
Answer: “The hazards presented by molds that may
contain mycotoxins should be considered the same as
other common molds which can grow in your house.
There is always a little mold everywhere—in the air
and on many surfaces. There are very few case
reports that toxic molds (those containing certain
mycotoxins) inside homes can cause unique or rare
health conditions such as pulmonary hemorrhage or
memory loss. These case reports are rare, and a
causal link between the presence of the toxic mold
and these conditions has not been proven. A com-
mon-sense approach should be used for any mold
contamination existing inside buildings and homes.
The common health concerns from molds include
hay fever-like allergic symptoms. Certain individuals
with chronic respiratory disease (chronic obstructive
pulmonary disorder, asthma) may experience diffi-
culty breathing. Individuals with immune suppres-
sion may be at increased risk for infection from
molds. If you or your family members have these
conditions, a qualified medical clinician should be
consulted for diagnosis and treatment. For the most
part, one should take routine measures to prevent
mold growth in the home.
Question: “What are the potential health effects of
mold in buildings and homes?”
Answer: “Mold exposure does not always present a
health problem indoors. However some people are
sensitive to molds. These people may experience
symptoms such as nasal stuffiness, eye irritation, or
wheezing when exposed to molds. Some people may
have more severe reactions to molds. Severe reac-
tions may occur among workers exposed to large
amounts of molds in occupational settings, such as
farmers working around moldy hay. Severe reactions
may include fever and shortness of breath. People
with chronic illnesses, such as obstructive lung dis-
ease, may develop mold infections in their lungs.
The mold neurotoxicity debate is not simply about health
care and science—money and litigation are salient in the
concerns of those claiming neuropsychological injuries are
caused by toxic mold. The campaign being waged to con-
vince people of the dangers of “toxic mold” deserves atten-
tion and efforts to understand the underlying concerns. But
bypassing scientific evidence in favor of wholesale dis-
semination of “toxic mold” rhetoric is not a neutral act. If
it turns out that these exposures are neuropsychologically
harmless, the strong claims and loud alarms sounded by
lawyers, doctors, and others will nonetheless have harmed
numerous victims. Who will be responsible for their pain
and suffering or emotional distress at being told they have
“chemical AIDS” or “significantly elevated risk of cancer”
or “permanent brain damage”? On the other hand, if we
discover evidence of causation of neuropsychological
deficits in this area, the findings need to be presented
widely in a forum most helpful to affected patients, not
through sensationalized hyperbole.
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The cure for misinformation is good information, but the
treatment is not easy. A substantial number of advocates
are ignoring science and making vigorous efforts to make
mold neurotoxicity appear real before we know the truth.
But sensationalism, unfounded conjecture, and manipula-
tion of perception are no substitute for facts. The way to
determine the effects of inhalation of mycotoxins and mold
spores is through high-quality, well-controlled, scientific
studies—not speculation in adversarial settings.
It is helpful to examine the flourishing concerns about mold
neurotoxicity through the lenses of texts and Internet resources
that explore mistaken arguments and ineffective science. Fasci-
nating and instructive source books for this purpose include
Angell, 1996; Fumento;
Gilovich, 1993; Huber;
Lynn, & Lohr;
Murray, Schwartz, & Lichter;
and Wildavsky.
On the Internet, see Quackwatch,
available at, the American Coun-
cil on Science and Health available at,
and Junk at
As of this writing in 2003, the answer to the question posed
to psychological and neuropsychological experts, whether
inhalation of mycotoxins or mold spores causes neuropsy-
chological impairment or mental disorders, is “We don’t
know.” However, healthy skepticism is in order. The poten-
tial field of investigation is so vast that clear answers will
not be established soon. Experts have estimated that there
are close to 100,000 recognized species of fungi.
the number of possible exposures under different environ-
mental circumstances to persons in dramatically different
mental and physical condition, one can speculate endless-
ly. But speculation is not evidence.
At present, there is no scientific basis for claiming that
individuals have suffered mental and emotional injuries by
inhalation of mold, mold spores, or mold metabolites,
including mycotoxins in residential or office environ-
ments. To the extent that experts are expressing conclu-
sions that mold inhalation in residences or offices caused
mental or emotional injuries or brain injury, their opinions
are speculation, possibilities, and guesses.
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... Some initial neuropsychological studies that have been conducted suggested exposure may have a detrimental direct and/or indirect adverse impact on cognitive functioning (Baldo, Ahmed, & Ruff, 2002;Gordon, Johanning, & Haddad, 1999). However, it appears that methodological limitations of existing research limit the ability to make more clearly informed statements regarding the effects of mold on human CNS and neuropsychological functioning (Lees-Haley, 2003). ...
... Other authors utilizing the MMPI-2 have also recently suggested there is likely a high percentage of malingering specifically in mold neurotoxicity cases (Lees-Haley, 2003;Stone, Boone, Carla, & Lessler, 2006). While the MMPI-2 Fake Bad Scale (FBS; Lees-Haley, English, & Glenn, 1991) has been shown to be sensitive to negative response bias among compensation seeking patients (Greiffenstein, Baker, Gola, Donders, & Miller, 2002;Larrabee, 2003;Tsushima & Tsushima, 2001), we did not have the individual item responses in many cases to analyze the true FBS for the present sample. ...
... Some initial neuropsychological studies that have been conducted suggested exposure may have a detrimental direct and/or indirect adverse impact on cognitive functioning (Baldo, Ahmed, & Ruff, 2002;Gordon, Johanning, & Haddad, 1999). However, it appears that methodological limitations of existing research limit the ability to make more clearly informed statements regarding the effects of mold on human CNS and neuropsychological functioning (Lees-Haley, 2003). ...
... Other authors utilizing the MMPI-2 have also recently suggested there is likely a high percentage of malingering specifically in mold neurotoxicity cases (Lees-Haley, 2003;Stone, Boone, Carla, & Lessler, 2006). While the MMPI-2 Fake Bad Scale (FBS; Lees-Haley, English, & Glenn, 1991) has been shown to be sensitive to negative response bias among compensation seeking patients (Greiffenstein, Baker, Gola, Donders, & Miller, 2002;Larrabee, 2003;Tsushima & Tsushima, 2001), we did not have the individual item responses in many cases to analyze the true FBS for the present sample. ...
... Aspergilloma (synonymous: mycetoma) is a localized form of aspergillosis with agglomeration of mold mycelia to form a fungal ball. It usually develops in preformed air spaces, e.g., tuberculous caverns, bronchiectasis, or malignant diseases (Latgé, 1999;Stevens et al., 2000). ...
... However, these works were criticized because of methodological weaknesses (McCaffrey and Yantz, 2005). No consistent proof can be deduced from the literature that the toxin concentrations occurring indoors can cause neurotoxic effects (Bush RK et al., 2006;Chapman et al., 2003;Gordon et al., 2004;Gordon et al., 2006;Khalili et al., 2005;Lees-Haley, 2003;Terr, 2009). ...
In April 2016, the German Society of Hygiene, Environmental Medicine and Preventative Medicine (Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin (GHUP)) together with other scientific medical societies, German and Austrian medical societies, physician unions and experts has provided an AWMF (Association of the Scientific Medical Societies) guideline ‘Medical diagnostics for indoor mold exposure’. This guideline shall help physicians to advise and treat patients exposed indoors to mold. Indoor mold growth is a potential health risk, even without a quantitative and/or causal association between the occurrence of individual mold species and health effects. Apart from the allergic bronchopulmonary aspergillosis (ABPA) and the mycoses caused by mold, there is only sufficient evidence for the following associations between moisture/mold damages and different health effects: Allergic respiratory diseases, asthma (manifestation, progression, exacerbation), allergic rhinitis, exogenous allergic alveolitis and respiratory tract infections/bronchitis. In comparison to other environmental allergens, the sensitizing potential of molds is estimated to be low. Recent studies show a prevalence of sensitization of 3-10% in the total population of Europe. The evidence for associations to mucous membrane irritation and atopic eczema (manifestation, progression, exacerbation) is classified as limited or suspected. Inadequate or insufficient evidence for an association is given for COPD, acute idiopathic pulmonary hemorrhage in children, rheumatism/arthritis, sarcoidosis, and cancer. The risk of infections from indoor molds is low for healthy individuals. Only molds that are capable to form toxins can cause intoxications. The environmental and growth conditions and especially the substrate determine whether toxin formation occurs, but indoor air concentrations are always very low. In the case of indoor moisture/mold damages, everyone can be affected by odor effects and/or impairment of well-being. Predisposing factors for odor effects can be given by genetic and hormonal influences, imprinting, context and adaptation effects. Predisposing factors for impairment of well-being are environmental concerns, anxieties, conditioning and attributions as well as a variety of diseases. Risk groups that must be protected are patients with immunosuppression and with mucoviscidosis (cystic fibrosis) with regard to infections and individuals with mucoviscidosis and asthma with regard to allergies. If an association between mold exposure and health effects is suspected, the medical diagnosis includes medical history, physical examination, conventional allergy diagnosis, and if indicated, provocation tests. For the treatment of mold infections, it is referred to the AWMF guidelines for diagnosis and treatment of invasive Aspergillus infections. Regarding mycotoxins, there are currently no validated test methods that could be used in clinical diagnostics. From the perspective of preventive medicine, it is important that mold damages cannot be tolerated in indoor environments.
... According to Kuiper-Goodman (1998) they are the most important chronic dietary risk factor, higher than synthetic contaminants, plant toxins, food additives, or pesticide residues. Indeed, cancer, kidney toxicity, immune suppression are well recognized to be connected to chronic mycotoxicoses (Bü nger et al., 2004;Fuchs and Peraica, 2005;Leese-Haley, 2003;Pitt, 2000;Sharma, 1993). Food quality and safety are topics which are widely and intensively studied by the scientific community. ...
Full-text available
Fungal food spoilage plays a pivotal role in the deterioration of food and feed systems and some of them are also able to produce toxic compounds for humans and animals. The mycotoxins produced by fungi can cause serious health hazards, including cancerogenic, immunotoxic, teratogenic, neurotoxic, nephrotoxic and hepatotoxic effects, and Kashin-Beck disease. In addition to this, fungal spoilage/pathogens are causing losses of marketable quality and hygiene of foodstuffs, resulting in major economic problem throughout the world. Nowadays, food spoilage can be prevented using physical and chemical methods, but no efficient strategy has been proposed so far to reduce the microbial growth ensuring public health. Therefore, lactic acid bacteria (LAB) can play an important role as natural preservatives. The protection of food products using LAB is mainly due to the production of antifungal compounds such as carboxylic acids, fatty acids, ethanol, carbon dioxide, hydrogen peroxide, and bacteriocins. In addition to this, LAB can also positively contribute to the flavor, texture, and nutritional value of food products. This review mainly focuses on the use of LAB for food preservation given their extensive industrial application in a wide range of foods and feeds. The attention points out the several industrial patents concerning the use of antifungal LAB as biocontrol agent against spoilage organisms in different fermented foods and feeds.
... Litigation status is an important, albeit controversial, factor in recovery from TBI. 7,31 Litigation status involves individuals who are seeking financial compensation for residual injuries following a TBI. This type of post-incident factor 32 can create a clinical syndrome in someone without any residual deficits, or distort a true clinical picture such that deficits and symptoms that normally would recover continue to be reported over time. ...
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Traumatic brain injury (TBI) is a neurological injury that can affect the cognitive, emotional, psychological, and physical functioning of an individual. The clinical neuropsychologist working with TBI patients must take a holistic approach when assessing and treating the patient and consider the patient in total, including premorbid and post-incident factors, to formulate a comprehensive and accurate picture of the patient. This approach will guide the clinician regarding multiple types of treatment the patient may require.
Die von der Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin (GHUP) federführend erstellte Leitlinie „Medizinisch klinische Diagnostik bei Schimmelpilzexposition in Innenräumen“ ist Gegenstand des vorliegenden Abschnitts. Schimmelpilzwachstum im Innenraum ist als ein potenzielles Gesundheitsrisiko zu betrachten, auch ohne dass ein quantitativer und/oder kausaler Zusammenhang zwischen dem Vorkommen einzelner Arten und Gesundheitsbeschwerden gesichert werden kann. Abgesehen von der Allergischen Bronchopulmonalen Aspergillose (ABPA) und den durch Schimmelpilze kausal verursachten Mykosen, liegen lediglich ausreichende Evidenzen für folgende Assoziationen von Feuchte-/Schimmelpilzschäden und unterschiedlichen Gesundheitseffekten vor: allergische Atemwegserkrankungen, Asthma (Manifestation, Progression, Exazerbation), allergische Rhinitis, Exogen Allergische Alveolitis, Begünstigung von Atemwegsinfekten/Bronchitis. Dabei ist das sensibilisierende Potenzial von Schimmelpilzen im Vergleich zu anderen Umweltallergenen deutlich geringer einzuschätzen. Aktuelle Studien zeigen europaweit eine vergleichsweise geringe Sensibilisierungsprävalenz von 3–10 % gemessen an der Gesamtbevölkerung. Eingeschränkte oder vermutete Evidenz für eine Assoziation liegt vor hinsichtlich „mucous membrane irritation“ und Atopischen Ekzems (Manifestation, Progression, Exazerbation). Inadäquate oder unzureichende Evidenz für eine Assoziation liegt vor für COPD, akute idiopathische pulmonale Hämorrhagie bei Kindern, Rheuma/Arthritis, Sarkoidose und Krebserkrankungen. Das Infektionsrisiko von den in Innenräumen regelmäßig vorkommenden Schimmelpilzarten ist für gesunde Personen gering, die meisten Arten sind in die Risikogruppe 1 und wenige in 2 (Aspergillus fumigatus, A. flavus) der Biostoffverordnung eingestuft. Nur Schimmelpilze, die potenziell in der Lage sind, Toxine zu bilden, kommen als Auslöser einer Intoxikation in Betracht. Ob im Einzelfall eine Toxinbildung im Innenraum stattfindet, entscheiden die Umgebungs- und Wachstumsbedingungen und hier vor allem das Substrat. Von Geruchswirkungen und/oder Befindlichkeitsstörungen kann bei Feuchte-/Schimmelpilzschäden im Innenraum grundsätzlich jeder betroffen sein. Hierbei handelt es sich nicht um eine Gesundheitsgefährdung. Prädisponierende Faktoren für Geruchswirkungen können genetische und hormonelle Einflüsse, Prägung, Kontext und Adaptationseffekte sein. Prädisponierende Faktoren für Befindlichkeitsstörungen können Umweltbesorgnisse, -ängste, -konditionierungen und -attributionen sowie eine Vielzahl von Erkrankungen sein. Besonders zu schützende Risikogruppen bezüglich eines Infektionsrisikos sind Personen unter Immunsuppression nach der Einteilung der Kommission für Krankenhaushygiene und Infektionsprävention (KRINKO) beim Robert Koch-Institut (RKI) und Personen mit Mukoviszidose (Zystischer Fibrose), bezüglich eines allergischen Risikos Personen mit Mukoviszidose (Zystischer Fibrose) und Personen mit Asthma bronchiale. Die rationale Diagnostik beinhaltet die Anamnese, eine körperliche Untersuchung, eine konventionelle Allergiediagnostik einschließlich gegebenenfalls Provokationstests, vereinzelt sind auch zelluläre Testsysteme indiziert. Zum Vorgehen bei Schimmelpilzinfektionen wird auf die angemeldete AWMF-Leitlinie Diagnose und Therapie invasiver Aspergillus-Infektionen verwiesen. Hinsichtlich Mykotoxine existieren zurzeit keine brauchbaren und validierten Testverfahren, die in der klinischen Diagnostik eingesetzt werden könnten. Präventivmedizinisch ist wichtig, dass Schimmelpilzbefall in relevantem Ausmaß aus Vorsorgegründen nicht toleriert werden darf. Zur Beurteilung des Schadensausmaßes und zum Vorgehen wird auf den „Schimmelpilzleitfaden“ des Umweltbundesamtes verwiesen.
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This article is an abridged version of the AWMF mould guideline “Medical clinical diagnostics of indoor mould exposure” presented in April 2016 by the German Society of Hygiene, Environmental Medicine and Preventive Medicine (Gesellschaft für Hygiene, Umweltmedizin und Präventivmedizin, GHUP), in collaboration with the above-mentioned scientific medical societies, German and Austrian societies, medical associations and experts. Indoor mould growth is a potential health risk, even if a quantitative and/or causal relationship between the occurrence of individual mould species and health problems has yet to be established. Apart from allergic bronchopulmonary aspergillosis (ABPA) and mould-caused mycoses, only sufficient evidence for an association between moisture/mould damage and the following health effects has been established: allergic respiratory disease, asthma (manifestation, progression and exacerbation), allergic rhinitis, hypersensitivity pneumonitis (extrinsic allergic alveolitis), and increased likelihood of respiratory infections/bronchitis. In this context the sensitizing potential of moulds is obviously low compared to other environmental allergens. Recent studies show a comparatively low sensitizing prevalence of 3–10% in the general population across Europe. Limited or suspected evidence for an association exist with respect to mucous membrane irritation and atopic eczema (manifestation, progression and exacerbation). Inadequate or insufficient evidence for an association exist for chronic obstructive pulmonary disease, acute idiopathic pulmonary hemorrhage in children, rheumatism/arthritis, sarcoidosis and cancer. The risk of infection posed by moulds regularly occurring indoors is low for healthy persons; most species are in risk group 1 and a few in risk group 2 (Aspergillus fumigatus, A. flavus) of the German Biological Agents Act (Biostoffverordnung). Only moulds that are potentially able to form toxins can be triggers of toxic reactions. Whether or not toxin formation occurs in individual cases is determined by environmental and growth conditions, above all the substrate. In the case of indoor moisture/mould damage, everyone can be affected by odour effects and/or mood disorders. However, this is not a health hazard. Predisposing factors for odour effects can include genetic and hormonal influences, imprinting, context and adaptation effects. Predisposing factors for mood disorders may include environmental concerns, anxiety, condition, and attribution, as well as various diseases. Risk groups to be protected particularly with regard to an infection risk are persons on immunosuppression according to the classification of the German Commission for Hospital Hygiene and Infection Prevention (Kommission für Krankenhaushygiene und Infektionsprävention, KRINKO) at the Robert Koch- Institute (RKI) and persons with cystic fibrosis (mucoviscidosis); with regard to an allergic risk, persons with cystic fibrosis (mucoviscidosis) and patients with bronchial asthma should be protected. The rational diagnostics include the medical history, physical examination, and conventional allergy diagnostics including provocation tests if necessary; sometimes cellular test systems are indicated. In the case of mould infections the reader is referred to the AWMF guideline “Diagnosis and Therapy of Invasive Aspergillus Infections”. With regard to mycotoxins, there are currently no useful and validated test procedures for clinical diagnostics. From a preventive medicine standpoint it is important that indoor mould infestation in relevant dimension cannot be tolerated for precautionary reasons. With regard to evaluating the extent of damage and selecting a remedial procedure, the reader is referred to the revised version of the mould guideline issued by the German Federal Environment Agency (Umweltbundesamt, UBA).
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Damage to human neurological system cells resulting from exposure to mycotoxins confirms a previously controversial public health threat for occupants of water-damaged buildings. Leading scientific organizations disagree about the ability of inhaled mycotoxins in the indoor environment to cause adverse human health effects. Damage to the neurological system can result from exposure to trichothecene mycotoxins in the indoor environment. This study demonstrates that neurological system cell damage can occur from satratoxin H exposure to neurological cells at exposure levels that can be found in water-damaged buildings contaminated with fungal growth. The constant activation of inflammatory and apoptotic pathways at low levels of exposure in human brain capillary endothelial cells, astrocytes, and neural progenitor cells may amplify devastation to neurological tissues and lead to neurological system cell damage from indirect events triggered by the presence of trichothecenes.
Throughout history, humans have fallen victim to a variety of neurotoxins, with exposures coming in the form of tainted products, industrial pollution, drugs of abuse, and even the bread and water that sustain them. Despite this long and tumultuous history, neurotoxic outbreaks still occur with regular frequency. Although many difficulties currently exist in linking many of today's unexplained neurologic disorders to toxins, the past suggests a prominent role for neurotoxins in diseases (such as amyotrophic lateral sclerosis and PD), unexplained peripheral neuropathies, neurodevelopmental disorders, and many psychiatric disturbances.
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The topic of building related illness came into the public's eye as a major health issue in the mid 1970s, when several cases of pneumonia were found to be associated with an infectious agent in Philadelphia. This agent was subsequently found to be a gram-positive bacterium known as Legionella pneumoniae. During the ensuing 30 years, a myriad of symptom constellations, disorders, clinical syndromes and illnesses have been attributed to indoor living or working environments. Over time, there appeared to be no limit to claims of building related illness, and it was "reported" that almost any kind of clinical symptom, real or imaginary, could be blamed on indoor environments. As society became more and more litigious, many of these disorders were erroneously played out in courtrooms rather than medical offices, creating a circus atmosphere surrounding this class of disorders. With the advent of the internet, as well as other advances in telecommunications, these issues eventually became part of a media frenzy, and all truths could be thrown out the window as issues became more and more decided upon by emotions and unfounded beliefs, rather than scientific data and logical thinking.
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This statement describes molds, their toxic properties, and their potential for causing toxic respiratory problems in infants. Guidelines for pediatricians are given to help reduce exposures to mold in homes of infants. This is a rapidly evolving area and more research is ongoing.
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This study investigated response bias in self reported history of factors relevant to the assessment of traumatic brain injury, toxic brain injury and related emotional distress. Response bias refers to systematic error in self report data. A total of 446 subjects comprising 131 litigating and 315 non litigating adults from five locations in the United States completed a symptom questionnaire. Data were obtained from university faculty and students, from patients in clinics specializing in physiatry, neurology, and family medicine, and from plaintiffs undergoing forensic neuropsychological evalua tions. Comparisons were made for litigant and non litigant ratings of their past and current cognitive and emotional functioning, including life in general, ability to concentrate, memory, depression, anxiety, alcohol, drugs, ability to work or attend school, irritability, headaches, confusion, self esteem, and fatigue. Although there is no basis for hypothesizing plaintiffs to be healthier than the general popul...
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• One-month prevalence results were determined from 18571 persons interviewed in the first-wave community samples of all five sites that constituted the National Institute of Mental Health Epidemilogic Catchment Area Program. US population estimates, based on combined site data, were that 15.4% of the population 18 years of age and over fulfilled criteria for at least one alcohol, drug abuse, or other mental disorder during the period one month before interview. Higher prevalence rates of most mental disorders were found among younger people (<age 45 years), with the exception of severe cognitive impairments. Men had higher rates of substance abuse and antisocial personality, whereas women had higher rates of affective, anxiety, and somatization disorders. When restricted to the diagnostic categories covered in international studies based on the Present State Examination, results fell within the range reported for European and Australian studies.
A 1998 meta-analysis by B. Rind, P. Tromovitch, and R. Bauserman in Psychological Bulletin indicated that the relations between child sexual abuse and later psychopathology were weak in magnitude. Shortly thereafter, this article was condemned by media personality Dr. Laura Schlessinger and numerous conservative organizations and was denounced by the United States Congress. In addition, the American Psychological Association (APA) distanced itself from the authors' conclusions. This incident raises questions regarding (a) authors' responsibilities concerning the reporting of politically controversial findings, (b) academic and scientific freedom, (c) the role of the APA in disabusing the public and media of logical errors and fallacies, and (d) the substantial gap between popular and academic psychology and the responsibility of the APA to narrow that gap.
In this study research participants completed the Minnesota Multiphasic Personality Inventory-2 (MMP1-2) under standard instructions and then were asked to fake posttraumatic stress disorder (PTSD) when completing the MMP1-2 for a 2nd time in 1 of 4 conditions with different instructions on how to fake PTSD: (a) uncoached, (b) coached about PTSD symptom information, (c) coached about MMP1-2 validity scales, or (d) coached about both symptoms and validity scales. These MMP1-2 protocols were then compared with protocols of claimants with workplace accident-related PTSD. Participants given information about the validity scales were the most successful in avoiding detection as faking. The family of F scales (i.e., F, F-B, F-P), particularly F-P, produced consistently high rates of positive and negative predictive power.
The controversy surrounding B. Rind, P. Tromovitch, and R. Bauserman (1998) prot,ides valuable lessons into scientific independence, politics, and organizational decision making. In an unprecedented action, the U.S. Congress officially condemned findings of Rind et at. Meanwhile, the American Psychological Association took similarly unprecedented measures in an effort to assuage its Congressional critics. This article, written from the perspective of a psychologist serving in Congress, discusses the various political and organizational dynamics that developed during the controversy. Understanding and learning from this incident can help psychologists and their professional associations better prepare for and respond to potential controversies arising from research or other publications.
Minnesota Multiphasic Personality Inventory (MMPI-2) validity scales were compared in 4 groups : nonclinical participants answering under standard instructions (n = 20), nonclinical participants instructed to fake closed-head injury (CHI) symptoms (n = 18), non-compensation-seeking CHI patients (n = 31), and compensation-seeking CHI patients (n = 30). The highest scores on MMPI-2 overreporting scales were obtained by nonclinical participants faking CHI, and significantly higher scores on these scales were obtained by compensation-seeking relative to non-compensation-seeking CHI patients. These results suggest that MMPI-2 overreporting scales are sensitive to fabrication of CHI complaints, and possibly to exaggeration of CHI complaints, although further research is necessary to evaluate the latter hypothesis fully.
A large sample of chronic postconcussive patients with and without overt malingering signs was compared with objectively brain-injured patients on common episodic memory and malingered amnesia measures. Probable malingerers and traumatically brain-injured Ss were not differentiated on popular episodic recall tests. In contrast, probable malingerers performed poorly on the Rey 15-item, Rey Word Recognition List, Reliable Digit Span, Portland Digit Recognition Test, and Rey Auditory Verbal Learning Test recognition trial. These findings validated both commonly cited malingering measures and newly introduced methods of classifying malingering in real-world clinical samples. The base rate for malingering in chronically complaining mild head injury patients may be much larger than previously assumed. (PsycINFO Database Record (c) 2012 APA, all rights reserved)
The postconcussion syndrome is a term invoked to describe a constellation of cognitive (decreased memory and concentration), emotional (increased irritability and nervousness or anxiety), and physical (increased headaches and dizziness) changes that are commonly reported following minor or severe head injuries. The first section presents the development and validation of the Postconcussion Syndrome Checklist. The second section describes the daily changes in symptom reports as a function of daily stress levels. A population of head-injured subjects and controls monitored postconcussion symptoms and stress across a 6-week period. The frequency, intensity, and duration of symptoms reported were correlated with daily stress levels as measured by the Daily Stress Inventory for both groups. Yet, the number of symptoms reported by our head-injured group did not vary significantly from the normal subjects. The data support models which predict that postconcussion syndrome varies with stress, but the evidence for a reduction in the cerebral reserve capacity after head injury was not supported with this population. Explanations for this finding are presented and implications of this research and directions for future research are outlined.