Health Effects Attributed to Mold

Heath Effects
Attributed To Mold
Harriet A. Burge,Ph.D.
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Outline
1. The immune system and how it relates to fungal
disease
2. Infection
3. Hypersensitivity
a. Allergies
b. Hypersensitivity pneumonitis
4. Toxicity

Immune System
Evolved to prevent infection
Plays a fundamental role in hypersensitivity diseases
Is damaged by some toxins

Immune System (cont’d)
• Development of all cells of the immune system
begins in the bone marrow with a blood-forming
stem cell
• Two broad categories of immune responses: the
innate immune system and the adaptive immune
system
• Central to both categories: the ability to distinguish
our own tissues (that need protection) from foreign
invaders (that need to be attacked)

Innate Immune Responses
• Rely on cells that require no additional “training” to
do their jobs. These cells include neutrophils,
monocytes, natural killer (NK) cells and a set of
proteins termed the complement proteins.
• Innate responses to infection occur rapidly and
reliably. Even infants have excellent innate immune
responses.

Adaptive Immune Responses
• Involve T-cells and B-cells, two cell types that
require “training” or education to learn not to attack
our own cells.
• The advantages of the adaptive responses are their
long-lived memory and the ability to adapt to new
germs.

Cells of the Immune System
• A. Bone marrow: most of
the cells of the immune
system are produced here as
immature or stem cells.
• B. Stem cells: have the
potential to differentiate and
mature into the different cells
of the immune system.
• C. Thymus: An organ
located in the chest that
instructs immature
lymphocytes (white blood
cells) to become matureT-
lymphocytes.

Cells of the Immune System (cont’d)
• D. B-Cells: These
lymphocytes differentiate into
plasma cells that produce
immunoglobulins
(antibodies).
• E. Cytotoxic T-cells:
lymphocytes that mature in
the thymus and are
responsible for killing
infected cells.
• F. Helper T-cells:
lymphocytes that “help” other
T-cells and B-cells to
perform their functions.

Cells of the Immune System (cont’d)
• I. Neutrophils
(Polymorphonuclear PMN
Cell): rapidly ingest
microorganisms and kills
them.
• J. Monocytes: develop into
macrophages when they
migrate to tissues.

Immunoglobulins (Antibodies)
• Proteins that bind specifically to a particular
substance—an antigen.
• All antibodies have the same overall structure
• Each antibody molecule has a unique structure that
enables it to bind specifically to its corresponding
antigen.
• Antibodies are produced by plasma cells in
response to infection, immunization, or allergen
exposure.

Antibodies
The two arms of the Y-
shaped antibody molecule
contain the variable regions
that form the two identical
antigen-binding sites.
The stem or constant
region engages the effector
mechanisms that
antibodies activate to
eliminate pathogens or
release symptom-causing
chemicals.

Infection – Colonization
• An infection occurs when a microbe enters the body
and begins to reproduce. The microbe must:
– Survive and multiply under local conditions (e.g. of
temperature and pH) to establish itself in its new habitat
– Successfully compete against the established indigenous
microbial flora
– Resist local defense mechanisms
• Once established on a body surface, an organism is
said to have colonized that site.

Infection
• The invading microbe may
– Remain dormant
– Directly damage cells, or
– Immune system can cause symptoms such as fever, as
it tries to rid your body of the invader.

Infection – Host Response
• Usually begins with an inflammatory reaction,
followed by a humoral or cell-mediated immune
response.
• Damage occurs due to swelling, increased fragility
of tissues, formation of pus, scarring or necrosis.
• Chronic intracellular infection may cause formation
of fibrous nodules and a state of latency from which
acute infection can be re-established at a much later
stage.

Classification of Mycoses
• The clinical nomenclatures used for the mycoses
are based on the
– (1) Site of the infection,
– (2) Route of acquisition of the pathogen, and
– (3) Type of virulence exhibited by the fungus.

Classification Based on Site of Infection
• Superficial,
• Cutaneous,
• Subcutaneous,
• Systemic (deep) infections
depending on the type and
degree of tissue involvement
and the host response to the
pathogen.

Mycoses

Classification Based on Route of
Acquisition
• Exogenous or endogenous routes of entry
– Airborne, cutaneous or percutaneous.
– Endogenous infection involves colonization by a member
of the normal flora or reactivation of a previous infection.

Classification Based on Virulence
• Primary pathogens can establish infections in
normal hosts.
• Opportunistic pathogens cause disease in
individuals with compromised host defense
mechanisms.
• The primary pathogens have relatively well-defined
geographic ranges; the opportunistic fungi are
ubiquitous.

Fungal Infections
• All require living spores for
disease
• Virulent agents do not
grow indoors and disease
depends on disturbance of
outdoor reservoirs
• Skin agents are probably
not airborne
• Opportunistic agents
common in the
environment

Primary (Virulent) Mycoses
• Able to cause infection in a normal host
– Coccidioides immitis
– Histoplasma capsulatum
– Blastomyces dermatitidis
– Paracoccidioides brasiliensis (South America)

Virulent Infections
• Histoplasmosis (Histoplasma capsulatum)
– Wet soil enriched with bird droppings
– Soil disturbance necessary for dissemination
– Endemic in the Mississippi valley
• Blastomycosis (Blastomyces dermatididis)
– Similar to Histoplasma
• Coccidioidomycosis (Coccidioides immitis)
– Dry desert soils
– Sandstorms

Virulent Fungal Infection
• Traveling to an area where the causative fungus is
common raises the risk for this infection.
• Serious infections occur in those with a weakened
immune system due to:
– Anti-tumor necrosis factor (TNF) therapy
– Cancer
– Chemotherapy
– Glucocorticoid medications (prednisone)
– Heart-lung conditions
– HIV
– Organ transplant
– Pregnancy (especially the first trimester)

Histoplasma capsulatum
• Etiologic agent of the most common respiratory
fungal infection affecting humans.
• Lives in the soil, usually in association with large
amounts of bird or bat droppings.
• Widely distributed throughout the subtropial and
tropical zones of the world. In North America, H.
capsulatum is particularly associated with the
Mississippi and Ohio River valleys.

Histoplasma capsulatum (cont’d)
• Exists in soil in a mycelial form
• Tuberculate macroconidia (8 to 14µm in diameter)
and microconidia (2-5 µm in diameter) are formed
in the soil
• Microconidia are likely the major source of infection
due to their small size, making them readily airborne
with soil disturbance, and able to penetrate to the
small airways of mammalian lungs by inhalation.

Histoplasma capsulatum (cont’d)
• In the body, H. capsulatum converts to a yeast form.
• Lung infection can occur after inhalation of airborne,
microscopic fungal spores when soil is disturbed.
• Many people who inhale the spores do not get sick.
• Symptoms of histoplasmosis are similar to
pneumonia, and the infection can sometimes
become serious if it is not treated.

Histoplasmosis
• Between 50% and 80% of people who live in areas
where Histoplasma capsulatum is common in the
environment will show evidence of having been
exposed to the fungus at some point in their lifetime.
In these areas, 10% to 25% of HIV-infected people
will develop disseminated histoplasmosis.
• There is a PCR assay for detection of H. capsulatum
in soil. Previously, soil suspensions had to be
inoculated into mice and (after 6 weeks or so) the
liver and spleen cultured.

Blastomyces dermatitidis (Blastomycosis)

Blastomyces dermatitidis (cont’d)
• Although long thought to be restricted to the North
American continent, cases have been diagnosed in
Africa, Asia and Europe in recent years.
• Clinical and epidemiological evidence indicates that
humans and lower animals contract blastomycosis
from some source in nature.
• However, the natural habitat of B. dermatitidis has
yet to be clearly delineated, despite some reports of
its isolation from soil.

Blastomycosis
• A true systemic (endemic) mycosis.
• Occurs mainly in immunocompetent hosts
• Acquired by inhalation and usually remains a lung
infection.
• Cutaneous infection occurs with direct inoculation of
the fungus into the skin.
• Dissemination to other organs and systems may
occur, especially in immunocompromised hosts.

Coccidioides immitis (Valley Fever)
• This fungus resides in soil
• Spores become airborne with disturbance (e.g., wind)

• Coccidioides is thought to
grow best in soil after heavy
rainfall and then disperse
into the air most effectively
during hot, dry conditions.
• Climate change may be
affecting the number of
Valley fever infections, as
well as the geographic
range of Coccidioides.
Coccidioides immitis (Valley Fever) cont’d

Coccidioides immitis (Valley Fever) cont’d
• Symptoms are flu-like, nonspecific and often
difficult to diagnose.
• Most people who breathe in the spores don’t get
sick. Usually, people who get sick will get better on
their own within weeks to months, but some people
will need antifungal medication.
• Immunocompromised people are at higher risk for
severe illness.
• Responsible for laboratory related infections where
the agent is handled.

Opportunistic Infections
• Are a serious issue for the
immune compromised:
– AIDS
– Organ transplants
– Chemotherapy
– Bone marrow transplants
• Not normally an issue for
people with competent
immune systems

Opportunistic Mycoses
• Candida albicans
• Aspergillus
• Zygomycetes (Rhizopus, Rhizomucor, Absidia,
Mucor sp.
• Cryptococcus neoformans and C. gattii

Candida albicans
• Candida is a resident organism in the human body.
• Infections are of endogenous origin (not
environmental)
• Illnesses:
– Thrush (mouth or throat)
– Yeast infection (genital area)
– Diaper rash (baby’s bottom)
– Invasive candidaisis (bloodstream)

Candida albicans (cont’d)
• Thrush
– Infants and the elderly
– Chemotherapy patients
– Patients with immunosuppressive disease
• Diaper rash
– Not always caused by Candida
– Can occur in any baby if bottom remains wet

Candidiasis or Candidemia
• You are more likely to get this invasive type of
infection if you:
– Are in the hospital's intensive care unit (ICU)
– Have had recent surgery
– Have a central line (catheter)
– Have a weakened immune system

Candida Infection on The Internet
• Some people with unexplained symptoms and
having a little information about Candida believe that
systemic candida infection has caused many
different symptoms both physical and psychological.
• Unfortunately, a few physicians have supported this
opinion.
• The key term is “believe.” There is no evidence for
such associations.

Aspergillus Infection
• All animals and many plants have
highly efficient mechanisms to
prevent themselves being infected
by Aspergillus, and it is usually only
when those mechanisms are
defective in some way that
Aspergillus can grow within the
body.
• Thus, this is a true opportunistic
infection

Invasive Aspergillosis
• Invasive aspergillosis (true Aspergillus infection) is
an important medical concern in
immunocompromised patients
• It is an airborne disease
• The number of living spores required to initiate an
infection is unknown, and probably varies with the
individual’s immune status.
• Millions of spores can be inhaled with no infection
occurring in normal people.

Aspergillus Infection (cont’d)
• Inhaled conidia germinate into invading hyphae that
penetrate the respiratory epithelium.
• Aspergillus traits, including the production of
pigment, antioxidants, proteases, adhesins,
siderophores, and mycotoxins, are implicated as
potential virulence factors.
• These factors interact in the patient with depressed
immunity to allow infection to occur.

Aspergillosis In General
• Invasive aspergillosis
– Invasive infection
• Aspergilloma
– colonization of “holes” in the lung parenchyma forming
Aspergillus balls
• Allergic bronchopulmonary aspergillosis
– Colonization of the mucous lining the lungs of asthmatics.
• Only invasive aspergillosis can be accurately called
an infection.

Zygomycetes
• Orders Mucorales and Entomophthorales include
human pathogens
• Entomophthorales infection is very rare
• Members of the Mucorales that cause human
disease:
– Rhizopus (most common)
– Mucor, Rhizomucor, Absidia, Apophysomyces,
Saksenaea, Cunninghamella, Cokeromyces, and
Syncephalastrum have also been causal agents.

Zygomycosis
• The spores are transmitted by
– inhalation,
– a variety of percutaneous routes,
– ingestion of spores.
• Opportunistic: Host risk factors include
– Diabetes mellitus, neutropenia, sustained
immunosuppressive therapy, chronic prednisone use, iron
chelation therapy, broad-spectrum antibiotic use, severe
malnutrition, and primary breakdown in the integrity of the
cutaneous barrier such as trauma, surgical wounds,
needle sticks, or burns.

Cryptococcus neoformans
• C. neoformans v. grubii and v. neoformans have a
worldwide distribution and are often found in soil
that has been contaminated by bird excrement.
• C. neoformans has been recovered from the ruins of
Chernobyl and may be able to use radiation as an
energy source.
• Cryptococcus is a basidiomycete belonging to the
order Tremelliales (jelly fungi). Basidiospores are
formed during a brief mycelial stage, and are
aerosolized, leading to possible inhalation exposure.

Cryptococcum neoformans
• C. neoformans is an opportunistic fungus. Normal
healthy people are rarely infected.
• Infections are usually pulmonary, although with
severe immunosuppression such as in AIDS
patients, meningioencephalitis can occur.
• Pulmonary cryptococcosis can be treated with
antifungal drugs.
• Central nervous system infections are very difficult
to treat and are often fatal.

Cryptococcus gattii
• Cryptococcus gattii, formerly known as
Cryptococcus neoformans var gattii, is a tropical
species, only recently reported in northeastern North
America.
• According to the CDC, from 2004 to 2010, 60 cases
were identified in the U.S.: 43 in Oregon, 15 from
Washington, and one each from Idaho and
California.
• About 52% of these were in immunocompromised
patients.

Skin Infections
• Microsporum, Epidermophyton, and Trichophyton
– Athlete’s foot
– Ringworm
– Jock itch

Infection – Cutaneous
• Microsporum, Epidermophyton, and Trichophyton
• Dermatophytes cause infections of the skin, hair and
nails, obtaining nutrients from keratinized material.
• Dermatophytes generally do not penetrate into living
tissue, but remain in the keratinized layer of the skin
• Common name for these infections include
ringworm, jock itch, athlete’s foot, and others
• Transmission is through direct contact with infected
people and shed fungal materials.

Hypersensitivity
• Immune responses to innocuous antigens that lead
to symptomatic reactions upon re-exposure
– Hypersensitivity: The state of heightened reactivity
to antigen.
– Hypersensitivity reactions are classified by mechanism:
• Type I reactions involve IgE antibody triggering of
mast cells;
• Type II reactions involve IgG antibodies against
cell surface or matrix antigens;
• Type III reactions involve antigen:antibody complexes;
• Type IV reactions are T cell-mediated.

Type I Hypersensitivity – Allergy

Mast Cells
• Large cells found in connective tissues throughout
the body, most abundantly in the submucosal
tissues and the dermis.
• Contain large granules that store mediator
molecules including histamine.
• Have high-affinity Fcε receptors (FcεRI) that allow
them to bind IgE monomers.
• Antigen-binding to this IgE triggers mast-cell
degranulation and mast-cell activation,
• Producing a local or systemic immediate
hypersensitivity reaction.

Ports of Antigen (Allergen) Entry
• Intravenous:
– General release of histamine
• Intradermal
– Local release of histamine
• Inhalation, upper airway
• Inhalation, lower airway
• Gastrointestinal
– Diffusion into blood stream
Anaphylaxis
Wheal and flare
Allergic rhinitis
Asthma
Diarrhea, vomiting
Urticaria, anaphylaxis

Type I Hypersensitivity – Allergic Diseases
• Diseases
– Allergic rhinitis (hay fever)
– Asthma
– Anaphylaxis
– Eczema (atopic dermatitis)
– Allergic bronchopulmonary
aspergillosis

Exposure To Fungal Allergens
• Exposure to fungal allergens is high, and
sensitization is common (at least 10% of the
population)
• As with most allergens, low doses over a long period
of time are likely needed for sensitization. Higher
doses for symptoms.
• Fungal sensitivity predisposes the patient to severe
asthma.

Outdoor Aerosol
Most fungal allergen exposure occurs outdoors

Cladosporium Growing in Condensation

Fungal Colonization
• Diseases
– Allergic bronchopulmonary aspergillosis (mycosis)
– Allergic Fungal Sinusitis
• Background
– ABPA: fungus colonizes mucous in the lung; Symptoms
caused by immune response to the fungus
– AFS: Fungus colonizes mucous in sinuses; Sinuses fill with
fungal hyphae and thick mucous produced in response to the
fungal allergens
– Risk depends on having chronic asthma or rhinitis
– Only a few fungi are involved

Evidence for Allergic Reactions
• Asthma:
– There is extensive evidence to
document that exposure to fungi
can precipitate asthma attacks,
and may be involved in the initial
development of asthma in some
circumstances.
• Childhood asthma studies
• Work related asthma studies

Interesting Point
• Asthma attack related to
fungi on mouth guard
(Glass et al., 2007)
– If mouth guard is used only at
school, the school
environment could be blamed
– If mold is found in a building,
the tendency is to blame the
mold for symptoms
– Important to consider other
possibilities, especially if only
one person is affected.

Type III and IV Hypersensitivity
• Hypersensitivity pneumonitis (also called allergic
alveolitis) is caused by a combination of type III and
IV hypersensitivity responses
• Exposure to antigen leads to production of specific
IgG molecules. These are called precipitating
antibodies.
• Re-exposure to antigen leads to formation of
antigen/antibody complexes that deposit in the
alveoli (small sacs in the lung.
• This is the Type III response

Hypersensitivity Pneumonitis
In addition:
• Early response to the antigen leads to an increase
in neutrophils and mononuclear cells in the alveoli
and small airways.
• These cells release proteolytic enzymes,
prostaglandins, and leukotrienes. The production
and release of interleukins, cytokines, growth
factors, and various other mediators from T
lymphocytes and macrophages play important roles
in hypersensitivity pneumonitis pathogenesis.

Pathophysiology
• The subacute, or intermittent, form:
– Produces well-formed granulomas, bronchiolitis with or
without pneumonia, and interstitial fibrosis
– This type (stage) can often be reversed by eliminating
exposure
• Chronic forms:
– Display chronic interstitial inflammation and alveolar
destruction (honeycombing)
– There is no good treatment for this form, and continuing
exposure can lead to death

Acute Symptoms
• Fever
• Chills
• Fatigue
• Breathlessness
• Chest tightness
• Cough

Exposures Leading To Hypersensitivity
Pneumonitis
• Acute HP
– Intense exposure to small particle organic dusts including
small fungal spores.
• Chronic HP
– Low level exposure to small particle antigens over a long
period.

Antigens Leading To HP
• Compost HP
• Malt worker lung
• Peat moss HP
Aspergillus
Aspergillus clavatus
Monocillium sp,
Compost
Moldy barley
Penicillium citreonigrum Peat moss
• Suberosis Penicillum frequentans Moldy cork dust
• Maple bark HP Cryptostroma corticale Moldy wood bark
• Wood pulp worker lung Alternaria species Moldy wood pulp
• Wood trimmer lung Rhizopus species Moldy wood trimmings
• Tree cutter lung Penicillium (3 species)
Paecilomyces sp.
Aspergillus niger
Rhizopus sp.
Aspergillus sp.
Wood chips from living
maple and oak tree
• Dry rot HP Merulius lacrymans Moldy rotten wood
• Sequoiosis Graphium species, Moldy wood dust

Antigens Leading To HP (Cont’d)
• Japanese summer-type HP
• Cheese washer lung
Trichosporon cutaneum
Pencillum casei
Damp wood and mats
Cheese casings
P.roqueforti
• Tobacco worker lung Aspergillus sp. Moldy tobacco
• Greenhouse HP Aspergillus sp.
Penicillium sp.
Cryptostroma corticale
Moldy soil
• Esparto grass HP Aspergillus fumigatus Moldy esparto
(used to produce ropes, canvas, sandals, mats, baskets, and paper paste)
• Soy sauce brewer lung Aspergillus oryzae Fermentation starter
for soy sauce

Toxic Fungal Metabolites
• Toxic mainly to bacteria: Antibiotics
• Toxic mainly to plants: Phytotoxins
• Toxic to the animal kingdom and produced by
macrofungi (mushrooms): Mushroom toxins
• Toxic to the animal kingdom and produced by
microfungi: Mycotoxins

Toxicosis Classification of Mycotoxins
• Classification schemes tend to reflect the training of
the person doing the categorizing.
– Clinicians: classification by organ affected
• hepatotoxins, nephrotoxins, neurotoxins, immunotoxins, etc
– Cell biologists: mechanism of action
• teratogens, mutagens, carcinogens, and allergens
– Organic chemists: chemical structure
• lactones, coumarins
– Et cetera

Acute vs. Chronic Toxicosis
• Acute toxicity
– Adverse effects of a substance that result either from a
single exposure or multiple exposures in a short space
of time (usually less than 24 hours).
• Chronic toxicity
– Prolonged (repeated) exposure to a substance
– Prolonged internal exposure because a substance remains
in the body for a long time
• Doses required for acute toxicity are generally much
higher than those for chronic toxicity.

Is A Disease Caused By Mycotoxin Exposure?
• Anecdotal evidence: Suspicion that mycotoxins
have caused symptoms
• Animal studies: Documentation that effects CAN
occur in animals
• Epidemiology: Association between exposure and
disease; Dose/response information
• Biological monitoring: Measurement of toxins or their
metabolites or adducts in body fluids

Anecdotal Evidence
• Many anecdotal reports of mycotoxin associated
illness in the lay press
– None supported by unbiased data
– (Unfortunately) the courts accept these as indicating better
than a 50/50 chance of a cause/effect relationship
• A few anecdotal reports in the peer reviewed
literature indicating the possibility of an association
– Most admit that the association is not documented
– The courts accept these as well

Animal Studies
• Many reports of animal studies of mycotoxin effects.
• Most seek to document mechanisms of action
• Those attempting dose/response effects use very
high doses (much higher than would be expected
from environmental exposure except by ingestion.
• Many of these studies are very well done, and
indicate that mycotoxins are, in fact, toxic.
• They do not establish a connection between
exposure and disease.

Epidemiological Studies
• Several epidemiological studies associate chronic
mycotoxin exposure with cancer. These are all
occupational.
• One epidemiological study reported associations
between Stachybotrys on walls of infant bedrooms
and pulmonary bleeding in the infants.
• The epidemiology in this study was improperly done,
and the same organization (CDC) published an
analysis of the former study, saying that the
conclusions were not justified.

Biological Monitoring
• Biological monitoring is commonly done in studies
documenting ingestion of mycotoxins. Most of these
are focused on whether or not particular populations
are routinely exposed to mycotoxins in their food.
• A few studies claim detection of mycotoxins in bodily
fluids of people reporting airborne residential
mycotoxin exposure. So far, these studies are not
convincing, primarily because of bias.

Lower Respiratory Infections
• Lower respiratory illness:
– There is epidemiological evidence
that children living in damp
buildings have an increased
incidence of lower respiratory
infections.
– These effects are separate from
asthma, and don’t depend on
sensitivity to the fungi, or to family
history of allergies.
– Some hypothesize that mycotoxins
are involved, but no good evidence
for this connection has appeared.

Anecdotal evidence: word of mouth, case studies
Experimental evidence Epidemiological evidence
Logic
“proof”
Types of Evidence

Fungal Irritants
• Irritants (volatile organic
compounds):
– There is some evidence that these
agents cause mucous membrane
(eye, nose) irritation, and may
lead to headaches.
– Evidence so far is incomplete but
there is no indication so far that
these effects do not occur.
– Neurological effects probably due
to perception of odors

Evidence for Fungal-Associated Irritant Effects
Experimental evidence Epidemiological evidence
Logic
“proof”

Fungal Toxins
• Diseases
– Cancer
– Immunosuppression
– Neurological effects
– Irritant effects
• Background
– All of these effects are related to
ingestion of moldy food.
– Cancer requires long term
exposure; exposure cumulative
– Other effects are immediate;
exposures not cumulative
– Inhalation very unlikely as an
exposure route

Fungus Mycotoxins Possible health effects
Alternaria alternata Tenuazoic acid Nephrotoxic,
hepatotoxic,
hemorrhagic
Aspergillus flavus,
A. parasiticus
Aflatoxins Mutagenic, carcinogenic,
hepatotoxic
Aspergillus fumigatus Fumitremorgens,
gliotoxin
Tumorgenic, cytotoxic
Cladosporium sp. Epicladosporic acid Immunosuppressive
Fusarium moniliforme Fumonisins Neuro, nephrotoxic and
hepatotoxic, carcinogen
Stachybotrys
chartarum (atra)
Satratoxins,
verrucarins, roridins
Immunosuppressive,
hemotoxic, hemorrhagic
Mycotoxins

Fungal Toxins – New Information
• New information
– Hundreds of publications on
dietary mycotoxins,
especially in underdeveloped
countries.
– No new publications that
provide evidence for airborne
mycotoxin exposure.
– Stachybotrys conidia require air
speeds 1,000 times higher than
those that normally prevail in
the indoor environment.
(Tucker et al. 2007)

Fungal Toxins (cont’d)
• Toxic molds on the web
– Many sites on the web claim
that scientists are
underreporting the dangers of
toxic mold.
– Position papers by major
medical organizations are
considered “biased”.
– Expert witnesses are
considered biased because
they are paid for presenting
their opinions.

Fungal Toxins (cont’d)
• Comments
– Medical groups should not rely on reviews
for position papers, only the published
peer reviewed research literature.
– Courts should not decide scientific
relevance of scientific literature. Position
papers are consensus documents of
experts in the field, and should be
considered authoritative.
– Just because scientists are often defense
witnesses does not mean they do not
know the facts. Experts are hired because
they do know the facts. These same
experts would be used by the plaintiffs if
the facts fit their cases.
– The fact remains that the exposure models
are relevant and there is no good evidence
for mycotoxin inhalation disease

• Synergistic effects
• Biomarkers, and background measurements of each
– (note dietary mycotoxins as confounder)
– (sensitivity of the marker)
• Ochratoxin A: 0.011-0.1/A. carbonarius conidium

Evidence for Fungal-Associated Mycotoxin
Effects (Inhalation)
Experimental evidence Only forAgriculture
Logic
“proof”

Toxicological References
• Eduard W. 2009. Fungal spores: A critical review of
the toxicological and epidemiological evidence as a
basis for occupational exposure limit setting.
CRITICAL REVIEWS IN TOXICOLOGY 39(10):
799-864
• Hardin BD, Robbins CA, Fallah P, Kelman BJ. 2009.
The Concentration of No Toxicologic Concern
(CoNTC) and Airborne Mycotoxins JOURNAL OF
TOXICOLOGY AND ENVIRONMENTAL HEALTH-
PART A-CURRENT ISSUES 72(9): 585-598

• Pasqualotto, AC. (Ed.) 2010 Chapter: Ben-Ami R, Kontoyiannis DP, 345-379
• Kim et al., Indoor Air 2007; 17: 153–163
• Pini et al.,2008
• Tucker et al., Indoor Air 2007; 17: 153–163
• Burr et al., 2007. Thorax;62:767–772.
• Fisk et al., Indoor Air 2007; 17: 284–296
• Holck et al., 2007. Basic & Clinical Pharmacology & Toxicology 101, 455-458
• Iverson et al., 2007. Eur J Clin Microbiol Infect Dis 26:879–886
• Nucci & Anaissie, 2007. CLINICAL MICROBIOLOGY REVIEWS, 695–704
• Wang et al., 2007. Pediatr Allergy Immunol : 18: 441–447
• Park et al., 2008. Environ Health Perspect 116:45–50.
• Glass et al., 2007. Gen Dent. 55(5):4a36-40
• Sautour et al., 2007. J Hosp Infect. Dec;67(4):367-73.
• Wicklow & Shotwell., 1983. Canadian J Microbiology. 29(1):1-5.
General References

General References (cont’d)
• Janeway CA Jr, Travers P, Walport M, et al. Immunobiology: Hypersensitivity
diseases. Available from: http://www.ncbi.nlm.nih.gov/books/NBK27136/
• http://www.niaid.nih.gov/topics/microbes/documents/microbesbook.pdf

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Locations Nationwide to Serve You
(Addresses on Following Slides)
WASHINGTON
OREGON
IDAHO
NEVADA
MONTANA
WYOMING
UTAH
ARIZONA
COLORADO
NEW
MEXICO
TEXAS
NORTH
DAKOTA
SOUTH
DAKOTA
NEBRASKA
KANSAS
OKLAHOMA
MINNESOTA
IOWA
MISSOURI
ARKANSAS
LOUISIANA
WISCONSIN
INDIANA
ILLINOIS
OHIO
KENTUCKY
TENNESSEE
GEORGIA
SOUTH
CAROLINA
NEWYORK
PENNSYLVANIA
MICHIGAN
MAINE
WEST
VIRGINIA
VIRGINIA
NORTH
CAROLINA
NEW
HAMPSHIRE
VERMONT
MARYLAND
RHODEISLAND
CONNECTICUT
NEWJERSEY
DELAWARE
MASSACHUSETTS
HAWAII

EMLab P&K Locations Near You
MicroLabs in bold are
AIHA Accredited as
documented by the
Scope of Accreditation
Certificate.
Arizona - Phoenix
1501 West KnudsenDrive
Phoenix, AZ 85027
phone: 800.651.4802
fax: 623.780.7695
AIHA LAP, LLC EMLAP# 102297
California - San Francisco
6000 Shoreline Ct, Suite 205
So. San Francisco, CA94080
phone: 866.888.6653
fax: 650.624.5371
New Jersey - Marlton
3000 Lincoln Drive East, SuiteA
Marlton, NJ 08053
phone: 866.871.1984
fax: 856.334.1040
M I C R O L A B S
L A B O R A T O R I E S
California - San Diego
8304 Clairemont Mesa Blvd.
Suite 103
San Diego, CA 92111
Phone: 866.465.6653
Colorado - Denver
4955 YarrowStreet
Arvada, CO 80002
phone: 800.651.4802
Florida - Ft.Lauderdale
6301 NW 5th Way
Suite 1410
Ft. Lauderdale, FL33309
phone: 877.711.8400
Georgia - Atlanta
6500 McDonough Dr.
Suite C-10
Norcross, GA30093
phone: 877.711.8400
Illinois - Chicago
1815 West DiehlRd.
Suite 800
Naperville, IL 60563
phone: 866.871.1984
Nevada - Las Vegas
6000 S. Eastern Ave.
Suite 5E
Las Vegas, NV 89119
phone: 866.888.6653
California -Glendale
1010 N. Central Ave.
Suite 390
Glendale, CA 91202
phone: 866.465.6653
California -Irvine
17461 Derian Ave.
Suite 100
Irvine, CA 92614
Phone: 866.465.6653
California -Sacramento
880 Riverside Parkway
West Sacramento, CA95605
phone: 866.888.6653
Texas - Houston
6310 Rothway St.
Houston, Texas 77040
phone: 800.651.4802
Virginia - Fairfax
3929 Old Lee Highway
Unit 91C
Fairfax, Virginia 22030
phone: 866.871.1984
Washington -Seattle
19515 North Creek
Parkway N, Suite 100
Bothell, WA98011
phone: 866.888.6653
For the most current list of locations, please visit us at www.emlab.com
Contact individual laboratories for service capabilities and scopes of accreditation.

TestAmerica Locations
For your convenience, you can drop off samples for EMLab P&K at these locations.
CALIFORNIA- Pleasanton
1220QuarryLn.
Pleasanton,CA94566
phone:(925)484-1919
CALIFORNIA- SanBernardino
202E.Airport Road
Suite140
SanBernardino,CA92408
Phone:(909)370-4707
CALIFORNIA–W.Sacramento
880RiversidePkwy
WestSacramento,CA95605
phone:(916)373-5600
CONNECTICUT
128LongHill CrossRd.
Shelton,CT06484
phone:(203)929-8140
FLORIDA- Jacksonville
8933WesternWay,Suite 1
Jacksonville,FL32256
phone:(904)519-9551
FLORIDA-Orlando
8010SunportDrive, Suite116
Orlando,FL32809
phone:(407)851-2560
FLORIDA- Pensacola
3355McLemoreDr.
Pensacola,FL32514
phone:(850)474-1001
FLORIDA - Tallahassee
2846 Industrial Plaza Dr.
Tallahassee,FL32301
phone:(850)878-3994
FLORIDA-Tampa
6712BenjaminRd.,Suite 100
Tampa,FL33634
phone:(813)885-7427
GEORGIA-Atlanta
6500McDonoughDrive, SuiteC-10
Norcross,GA30093
phone:(678)966-9991
GEORGIA- Savannah
5102LaRocheAvenue
Savannah,GA31404
phone:(912)354-7858
HAWAII- Honolulu
99-193AieaHeightsDr.
Suite121
Aiea,HI96701
phone:(808)486-5227
ILLINOIS-Chicago
2417BondStreet
UniversityPark,IL60484
phone:(708)534-5200
ILLINOIS-Elmhurst
655W.GrandAve.,Suite 205
Elmhurst,IL60126
phone:(630)758-0262
INDIANA- Indianapolis
StutzBusinessCenter
212W.10thStreet,SteA-205
Indianapolis,IN46202
Phone:(317)264-9686
INDIANA-Valparaiso
2400CumberlandDrive
Valparaiso,IN46383
phone:(219)464-2389
IOWA-CedarFalls
704EnterpriseDrive
CedarFalls,IA50613
phone:(319)277-2401
IOWA-Davenport
736FederalSt.,Suite 2202
Davenport,IA52803
phone:(563)323-7944
LOUISIANA-Baton Rouge
6113BenefitDr.
BatonRouge,LA70809
phone:(225)755-8200
MARYLAND -Baltimore
5710ExecutiveDrive,Suite 106
Baltimore,MD21228
phone:(410)869-0085
MASSACHUSETTS-Boston
240BearHill Rd.,Suite 104
Waltham,MA02451
phone:(781)466-6900
MASSACHUSETTS-Westfield
53SouthamptonRoad
Westfield,MA01085
phone:(413)572-4000
MICHIGAN- Brighton
10448Citation Drive, Suite200
Brighton,MI48116
Phone:(810)229-2763
MINNESOTA- Minneapolis 7204
West27thStreet,Suite114 St.
LouisPark,MN55426 phone:
(800)593-8519
ALABAMA-Mobile
900LakesideDrive
Mobile,AL36693
phone:(251)666-6633
ALASKA -Anchorage
2000W.International Airport
Rd.,SuiteA10
Anchorage,AK99502
phone:(907)563-9200
ARIZONA- Phoenix
4625E.CottonCenterBlvd.,
Suite189
Phoenix,AZ85040
phone:(602)437-3340
ARIZONA- Tucson
1870W.PrinceRoad,Suite 59
Tucson,AZ85705
phone:(520)807-3801
CALIFORNIA–CostaMesa
3585CadillacAve,SuiteA
CostaMesa,CA92626
phone:(714)258-8610

TestAmerica Locations (cont’d)
NEWYORK-Albany
25KraftAve.
Albany,NY12205
phone:(518)438-8140
NEWYORK-Buffalo
10HazelwoodDrive, Ste. 106
Amherst,NY14228
phone:(716)691-2600
NEWYORK-NewYorkCity
47-3232ndPlace,Suite1141
LongIslandCity, NY11101
Phone:(347)507-0579
NEWYORK-Syracuse
118BossRd.
Syracuse,NY13211
phone:(315)431-0171
NORTHCAROLINA-Charlotte
I-85SouthBldg.
2858QueenCity Dr.,SuiteB
Charlotte,NC28208
phone:(704)392-1164
NORTHCAROLINA- Raleigh
101-FWoodwindsIndustrial Court
Cary,NC27511
phone:(919)380-9919
For your convenience, you can drop off samples for EMLab P&K at these locations.
OHIO- Cincinnati
11416ReadingRoad
Cincinnati, OH45241
phone:(513)733-5700
OHIO- Dayton
4738GatewayCircle
Dayton,OH45440
Phone:(937)294-6856
OHIO- NorthCanton
4101ShuffelStreetNW
NorthCanton,OH44720
phone:(330)497-9396
OREGON-Portland 9405
SWNimbusAvenue
Beaverton,OR97008
phone:(503)906-9200
PENNSYLVANIA-KingofPrussia
1008W.Ninth Ave.
KingofPrussia,PA19406
phone:(610)337-9992
PENNSYLVANIA-Pittsburgh
301AlphaDrive
Pittsburgh,PA15238
phone:(412)963-7058
SOUTHCAROLINA- Charleston
1436-ANorthPointLane
Mt.Pleasant,SC29464
phone:(843)849-6550
TENNESSEE-Knoxville
5815MiddlebrookPike
Knoxville,TN37921
phone:(865)291-3000
TENNESSEE-Nashville
2960FosterCreightonDr.
Nashville, TN37204
phone:(615)726-0177
TEXAS -Austin
14050SummitDr.,Ste.A100
Austin,TX78728
phone:(512)244-0855
TEXAS-Beaumont
4400LawndaleAve.
Groves,TX77619
phone:(409)540-5302
TEXAS-CorpusChristi
1733N.PadreIslandDrive
CorpusChristi, TX78408
phone:(361)289-2673
MISSOURI- Eureka
1699WestFifthStreet, #200
Eureka,MO63025
Phone:(314)302-8354
MISSOURI- KansasCity
601NW39thStreet
BlueSprings,MO64015
phone:(800)276-1286
MISSOURI -St.Louis
13715RiderTrailNorth
EarthCity, MO63045
phone:(314)298-8566
NEW JERSEY - Edison
777 NewDurham Road
Edison,NJ08817
phone:(732)549-3900
NEWJERSEY-SouthJersey
520FellowshipRd.,SuiteA-106
Mt.Laurel,NJ08054
phone:(856)222-1990
TEXAS -SanAntonio
404E.Ramsey,Suite208
SanAntonio,TX78216
phone:(210)344-9751
VERMONT -Burlington
30CommunityDrive, Suite11
SouthBurlington,VT05403
phone:(802)660-1990
VIRGINIA-VirginiaBeach
5135ClevelandStreet
VirginiaBeach,VA23462
phone:(757)671-1291
WASHINGTON-Richland
2800GeorgeWashingtonWay
Richland,WA99354
phone:(509)375-3131
WASHINGTON-Spokane
11922E.1stAve.
Spokane,WA99206
phone:(509)924-9200
WASHINGTON- Tacoma
57558thStreetEast
Tacoma,WA98424
phone:(253)922-2310

When quality and accuracy are critical.
Copyright © 2016 EMLab P&K, a TestAmerica Company
Analytical Services: Fungi, Asbestos, Bacteria, USP <797>, PCR, Allergens & Radon
Phone: (866) 888-MOLD (6653)
Email: info@emlabpk.com
Web: www.emlabpk.com

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