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Learn about how common mold mycotoxins can impact health in a dire manner, per the US Military. The following refers to battlefield and agricultural conditions, but the readers will note how similar many of these symptoms are to those, very tragically, experienced in many of our mold-contaminated, damp buildings - particularly, our schools (SMH).
Chapter 34
TRICHOTHECENE MYCOTOXINS
ROBERT W. WANNEMACHER, JR., PH.D.*; AND STANLEY L. WIENER, M.D.
INTRODUCTION
HISTORY AND MILITARY SIGNIFICANCE
Use in Biological Warfare
The Yellow Rain Controversy
Weaponization
DESCRIPTION OF THE AGENT
Occurrence in Nature
Chemical and Physical Properties
TOXICOLOGY AND TOXICOKINETICS
Mechanism of Action
Metabolism
CLINICAL DISEASE
Acute Effects
Chronic Toxicity
DIAGNOSIS
Battlefield Diagnosis
Confirmatory Procedures
MEDICAL MANAGEMENT
Individual and Unit
Specific or Supportive Therapy
Prophylaxis
SUMMARY
[Dangers of trichothecene mycotoxins (found in several common school molds), some excerpts from the US Military Manual, Ch. 34](SMH):
"This family of mycotoxins causes multiorgan effects including emesis and diarrhea, weight loss, nervous disorders, cardiovascular alterations, immunodepression, hemostatic derangements, skin toxicity, decreased reproductive capacity, and bone marrow damage.4,6
...In [Ch. 34] we will concentrate on T-2 mycotoxin, a highly toxic trichothecene that, together with some closely related compounds, has been the causative agent of a number of illnesses in humans and domestic animals.1,2
The trichothecene mycotoxins are toxic to humans, other mammals, birds, fish, a variety of invertebrates, plants, and eukaryotic cells in general... Once the trichothecene mycotoxins enter the systemic circulation, regardless of the route of exposure, they affect rapidly proliferating tissues.1,2,4,6,35,42,45 (Borden Institutute, US Army, Chapter 34
TRICHOTHECENE MYCOTOXINS, page 660)
T-2 Toxin: "Disease: Alimentory Toxic Aleukia; Agent: Trichothecene Mycotoxins; Producing Organisms: Fusarium & various other fungi; Entry route: Ingestion, Dermal & Inhalation; Toxic Response: Minutes to Days; Symptoms: blurred vision, hemorrhaging mucous membranes, dizziness, ataxia, tachycardia, hypothermia and hypotension; can induce DNA damage and cell death. Additional possible health effects include hemmorrhagic, immunosuppressive reactions as well as nausea and vomiting".
...the primary toxic effects of the trichothecene mycotoxins is caused by their properties as potent inhibitors of protein synthesis.
Although initial investigations on the mechanism of action of the trichothecene mycotoxins suggested that the inhibitionof protein synthesis as the principal mechanism of action, the above observations indicate that the effects of these toxins are much more diverse.
The lipophilic nature of these toxins suggests that they are easily absorbed through skin, gut, and pulmonary mucosa.
Mice, rats, and guinea pigs die rapidly (within 112 h) after exposure to high concentrations of aerosolized mycotoxin,with no apparent lung lesions or pulmonary edema.2830 This finding is in contrast to the effect of an oral dose of T-2 toxin, which causes direct damage to the intestinal mucosa.55 From these data, we can conclude that the trichothecene mycotoxins very rapidly cross the pulmonary and intestinal mucosa and enter the systemic circulation to induce the toxin-related toxicoses.In contrast, trichothecene mycotoxins are only slowly absorbed through skin, especially when applied as a dust or powder.56 Systemic toxicity and lethality can be produced by dermal exposure to higher concentrations of T-2 toxin, however, especially if the mycotoxin is dissolved in a penetrant such as DMSO.6
The degree of illness in an individual exposed to trichothecene mycotoxins could be affected by a
number of factors, including the nutritional status of the host, liver damage, intestinal infections, route
of toxin administration, and stress. The pathological effects and clinical signs for
many toxic materials can vary with the route and type (acute, single dose vs chronic, subacute doses)
of exposure. For the trichothecene mycotoxins, however, a number of the toxic responses are similar,
regardless of the route of exposure. As we discussed earlier in this chapter, once they enter the
systemic circulation, trichothecene mycotoxins affect rapidly proliferating tissue regardless of the
route of exposure. In contrast, the symptoms and clinical signs of
trichothecene intoxication can vary depending on whether the exposure is acute or chronic. Acute
exposure to trichothecene mycotoxins used as biological warfare agents is the major concern for military
medicine, but for continuity and historical implications, chronic intoxication will also be addressed
in this chapter.
Acute Effects
Acute oral, parenteral, dermal, or aerosol exposures
to trichothecene mycotoxins produce gastric
and intestinal lesions. Hematopoietic and immunosuppressive
effects are radiomimetic. Central
nervous system toxicity causes anorexia, lassitude,
and nausea; suppression of reproductive organ
function; and acute vascular effects leading to hypotension
and shock. While a number of toxic effect
are common to different routes of exposure,
route-specific effects have been observed in animal
models. Examples of local, route-specific effects
include the following:
dermal exposure: local cutaneous necrosis
and inflammation6;
oral exposure: lesions to the upper gastrointestinal
tract64; and
ocular exposure: corneal injury.6
Dermal Exposure
Similar cutaneous irritations have been observed
in numerous accidental and experimental settings:
Individuals who were exposed to hay or
hay dust contaminated with trichotheceneproducing
molds developed severe cutaneous
irritations.38
In working up large batches of fungal cultures
from trichothecene-producing organisms,
laboratory personnel suffered facial
inflammation followed by desquamation of
the skin and considerable local irritation.65
When trichothecene mycotoxins of relatively
low toxicity (crotocin and trichotecin)
were applied to the volar surface of
human forearm or to the human head, reddening
and irritation occurred within a few
hours of exposure, and was followed by
inflammation or scrabbling that healed in
1 to 2 weeks.66
The hands of two laboratory workers were
exposed to crude ethyl acetate extracts containing
T-2 toxin (approximately 200 μg/
mL) when the extract accidently got inside
their plastic gloves.66 Even though the
workers thoroughly washed their hands
with a mild detergent within 2 minutes after
contact, they experienced severe cutaneous
irritations.
These observations provide evidence that when
human skin is exposed in vivo to small amounts of
trichothecene mycotoxins, severe cutaneous irritations
develop and can last 1 to 2 weeks after acute
exposure.
A number of animal models have been used
to assess local and systemic toxicity and lethality
from skin exposure to trichothecenes.6 In a dermal
study that used a mouse model, necrosis in the skin
was present by 6 hours after dermal application.
Respiratory Exposure
Victims of yellow rain reported a variety of upper
respiratory signs and symptoms.7,27 The major
subdivisions of the respiratory tract that were affected
include the nose (itching, pain, rhinorrhea,
and epistaxis); the throat (sore/pain, aphonia, and
voice change); and the tracheobronchial tree (cough,
hemoptysis, dyspnea, and deep chest pain or pressure
or both). Agricultural workers who were exposed
to hay or hay dust contaminated with trichothecene
mycotoxins developed similar signs and
symptoms of upper respiratory injury. The descriptions
of the yellow rain attacks in Southeast Asia
(ie, the droplets, heavy mist, vapor), suggest that
the aerosols were larger than 1 to 4 μmthe particle
size required for deposition in the alveoli.
Thus, respiratory tract exposure from the largerparticle
aerosols would involve mycotoxin deposition
in the upper respiratory and tracheobronchial
region, followed by secondary gastrointestinal tract
exposure after clearance from the lungs.
The symptoms of
vomiting, diarrhea, melena, abdominal pain, and
acute gastroenteritis with hematemesis7 could be
related to ingestion of toxin that was deposited in
the upper respiratory tract and tracheobronchial
region.
In humans,
many of the acute enteral effects (from either yellow
rain or contaminated hay and dust particles)
of the trichothecene mycotoxins are probably the
result of secondary ingestion of toxins that originally
were deposited in the respiratory tract by
large-particle aerosol.
Chronic Toxicity
Chronic exposure to subacute doses of trichothecene
mycotoxins is not thought to be an effect of
biological warfare. This type of exposure, however,
was responsible for ATA toxicosis in humans and
mycotoxicosis in domestic animals. In addition,
chronic toxicity has been iatrogenically induced when
repeated subacute doses of a trichothecene mycotoxin
were administrated intravenously to cancer patients
as a chemotherapy for colon adenocarcinoma.
DIAGNOSIS (battlefield)
The early signs and symptoms of an
aerosol exposure to trichothecene mycotoxins
would depend on particle size and toxin concentration.
For a large-particle aerosol (particles > 10
μm, found in mist, fog, and dust; similar to that
used in Southeast Asia), the signs and symptoms
would include rhinorrhea, sore throat, blurred vision,
vomiting, diarrhea, skin irritation (burning
and itching), and dyspnea. Early (08 h) signs and
symptoms from a deep-respiratory aerosol exposure
(from aerosol particles in the 1- to 4-μm range) have
not been fully evaluated but could include vomiting,
diarrhea, skin irritation, and blurred vision.
Later signs and symptoms (824 h) would probably
be similar (except for the degree of skin rash
and blisters) for both large-particle and deeprespiratory
aerosol exposure to trichothecene mycotoxins.
They could include continued nausea and
vomiting, diarrhea, burning erythema, skin rash
and blisters, confusion, ataxia, chills, fever, hypotension,
and bleeding.
http://www.bordeninstitute.army.mil/published_volumes/chemBio/Ch34.pdf (Borden Institute, Textbooks of Military Medicine, Medical Aspects of Chemical and Biological Warfare, TRICHOTHECENE MYCOTOXINS, Ch. 34. Click here for a .pdf of this document.
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Satratoxin H: "Description: Mycotoxin; Fungus: Stachybotrys chartarum; this family of mycotoxins has a very high cytotoxicity" [toxicity to cells] (Aerotech P&K, Biological Warfare Agents, Microbial Toxins).
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