Re: stupid question on mycotoxins

[Guest guest]

You may want to check out www.mold-help.org and check

under fungi,mycotoxins,current research.

Barb E

--- moldhelp@... wrote:

> I am a bit of a dunce here and I am not getting

> mycotoxins. I do know

> however that they are produced in certain conditions

> and they are poisonous.

>

> Could someone explain or point me to a website that

> explains HOW they are

> toxic, what organs they attack, and what can be done

> to get rid of them

> (besides avoidance). Maybe even symptoms ?

>

> Thanks

> Angelika

>

>

>

____________________________________________________

Start your day with - make it your home page

http://www./r/hs

[Guest guest]

You can also try www.mycotoxicosis.com

> I am a bit of a dunce here and I am not getting mycotoxins. I do know

> however that they are produced in certain conditions and they are

poisonous.

>

> Could someone explain or point me to a website that explains HOW

they are

> toxic, what organs they attack, and what can be done to get rid of

them

> (besides avoidance). Maybe even symptoms ?

>

> Thanks

> Angelika

[Guest guest]

Date: Wed, 20 Jul 2005 23:10:58 -0700

From: <moldhelp@...>

Subject: stupid question on mycotoxins

I am a bit of a dunce here and I am not getting mycotoxins. I do know

however that they are produced in certain conditions and they are poisonous.

Could someone explain or point me to a website that explains HOW they are

toxic, what organs they attack, and what can be done to get rid of them

(besides avoidance). Maybe even symptoms ?

Thanks

Angelika

One interesting article can be found at http://www.wisc.edu/fri/fusarium.htm

Also, Aerotech Labs Tech Tip #35 discusses mycotoxins:

Potential Mycotoxins in Indoor Environments: IAQ Tech Tip #35

Exposure to saprophytic fungi (molds) in indoor environments has been linked

to a number of adverse health effects including, but not limited to,

lethargy, allergies, asthma, infection, dermatitis and hypersensitive

pneumonitis. While the aforementioned symptoms are intuitive and largely

recognized by both the scientific and lay communities, there are significant

secondary health effects associated with exposure to fungi, including

idiopathic pulmonary hemosiderosis in infants, cytotoxicity, cognitive

impairment, encephalopathies, immunosuppression, and cancer.

Research indicates that these secondary health effects may be caused by the

mycotoxins produced by the fungi. Although still controversial, in the end

mycotoxins may prove to be major components in the health effects reported

by victims of fungal exposure. Below are listed some of the more likely

mycotoxins that may occur in indoor environments as indicted by ACGIH, the

producing organisms, and mode of activity.

Aflatoxins are produced by Aspergillus flavus, and other Aspergillus spp.

Health effects: forms DNA adducts, hepato-toxic, carcinogenic, immunotoxic.

Alternariol is produced by Alternaria spp. Health effects: cytotoxic,

teratogenic.

Citrinin is produced by Penicillium expansum. Health effects: carcinogenic.

Chaetoglobosins is produced by Chaetomium globosin. Health effects:

inhibits cell division.

Cytochalasins is produced by Aspergillus clavatus. Health effects: inhibits

cell division.

Epicladosporic acid is produced by Cladosporium spp. Health effects:

immunosuppressive.

Fumonisins is produced by Fusarium spp.

Health effects: inhibits sphingolipid biosynthesis, neurotoxic, hepatotoxic,

nephrotoxic, carcinogenic.

Fumitremorgens is produced by Aspergillus fumigatus. Health effects:

tremorgenic.

Gliotoxin is produced by Aspergillus fumigatus.

Health effects: blocks membrane tiol groups, immunosuppressive,

cytotoxic.

Griseofulvins is produced by Memnoniella, P. griseo-fulvum and P.

viridicatum.

Health effects: hepatotoxic, tumorigenic, teratogenic.

Mycophenolic acid is produced by Penicillium brevicompactum.

Health effects: blocks inosine monophosphate dehydrogenase,

immunosuppressive.

Ochratoxins are produced by Aspergillus ochraceus and Penicillium

viridicatum.

Health effects: forms DNA adducts, inhibits protein synthesis

(phenyalanyl-t-RNA synthetase), nephrotoxic, carcinogenic.

Patulin is produced by Paecilomyces variatii and P. expansum.

Health effects: inhibits potassium uptake, possible carcinogen.

Trichothecenes - satratoxins, verrucarins, and roridins are produced by

Stachybotrys chartarum and Fusarium spp.

Health effects: inhibits protein and nucleic acid synthesis,

immunosuppressive, hemotoxic, hemorrhagic.

Sporidesmin is produced by Pithomyces chartarum. Health effects:

hepatotoxic.

Stachybotrylactams and lacones are produced by Stachybotrys chartarum.

Health effects: immunosuppressive.

Sterigmatocystin is produced by Aspergillus versicolor. Health effects:

hepatotoxic, carcinogenic.

Tenuazoic acid is produced by Alternaria alternata and Phoma soghina.

Health effects: nephrotoxic, hepatotoxic, hemorrhagic.

Verrucosidin is produced by Penicillium polonicum. Health effects:

neurotoxic.

*Data from Burge and Ammann (1999) and sen et al., 1993.

Burge, H. A. and Ammann, H. A., 1999. Fungal Toxins and b-(1®3)-D-Glucans.

Bioaerosols: Assessment and Control, Edited by J. Macher, H. A. Ammann, H.

A. Burge, D. K. Milton, and P. R. Morey (American Conference of Governmental

Industrial Hygienists, Cincinnati, Ohio), pp. 24-1 - 24-13.

sen, B. J., Bowen, K. L., Shelby, R. A., Diener, U. L. Kemppainen,

B.W., and Floyd, J. 1993. Mycotoxins and Mycotoxicoses. Circular ANR-767

(Alabama ative Extension Service), 16 pp.

[Guest guest]

Date: Wed, 20 Jul 2005 23:10:58 -0700

From: <moldhelp@...>

Subject: stupid question on mycotoxins

I am a bit of a dunce here and I am not getting mycotoxins. I do know

however that they are produced in certain conditions and they are poisonous.

Could someone explain or point me to a website that explains HOW they are

toxic, what organs they attack, and what can be done to get rid of them

(besides avoidance). Maybe even symptoms ?

Thanks

Angelika

JAMA. 2002;287:425-427)

Linking Evidence and Experience

Mycotoxins

Ruth A. Etzel, MD, PhD

Mycotoxins, chemicals produced by fungi, may have developed to serve as a

chemical defense system against insects, microorganisms, nematodes, grazing

animals, and humans. Approximately 400 known mycotoxins exist. This article

describes the major mycotoxins that affect human health and highlights the

mycotoxins with potential bioterrorist use.

Mycotoxins can benefit humans by their use as antibiotics (penicillins),

immunosuppressants (cyclosporine), and in control of postpartum hemorrhage

and migraine headaches (ergot alkaloids). Mycotoxins are also capable of

producing illness and death in humans and animals. Table 1 lists 4 major

classes of mycotoxins and their health effects.

Exposure to mycotoxins may occur through ingestion, inhalation, and dermal

exposure. 1, 2 The mycotoxins were discovered when epidemics of illness were

traced to ingestion of moldy food. Massive mycotoxin contamination of food

resulting in outbreaks of illness occurs only rarely today in developing

countries. The primary concern in developed countries is the long-term

effects of ingesting food contaminated with low levels of mycotoxins.

Although ergot alkaloids are described here because of their historical

importance, today the most commonly encountered mycotoxins in animal feed

and human foods are aflatoxins, fumonisins, and deoxynivalenol (vomitoxin).

Aflatoxins

Aflatoxins, produced by Aspergillus flavus and A parasiticus, are common

contaminants of peanuts, soybeans, grains, and cassava (a root), especially

in tropical areas. In the 1960s, aflatoxins were found to be potent

carcinogens in animals, 3 the most potent of which is aflatoxin B1.

Epidemiologic studies have demonstrated that aflatoxin B1 ingestion is an

important risk factor for hepatocellular cancer in humans. 4 Persons with

both hepatitis B infection and aflatoxin B1 exposure have a higher risk for

hepatocellular cancer than those with only hepatitis B infection or only

aflatoxin exposure. 5 In Qidong, Jiangsu Province, China, hepatocellular

carcinoma is the leading cause of cancer deaths and exposure to dietary

aflatoxins is widespread. Ongoing clinical trials there indicate that

oltipraz, an antischistosomal drug, can decrease the metabolism of aflatoxin

B1 to its carcinogenic form and increase the detoxification pathways of its

metabolites.6 Intervention with drugs such as oltipraz and improved storage

conditions of staple foods are measures under investigation to reduce the

incidence of hepatocellular cancer in regions of higher risk. 7

In addition to chronic effects, aflatoxin exposure can sometimes result in

acute aflatoxicosis with vomiting, abdominal pain, hepatitis, and death.

Although acute toxicity is rare, epidemics have been reported following

ingestion of food heavily contaminated with A flavus. 8 The acute lethal

dose for adults is 10 to 20 mg of aflatoxin.

Ergot Alkaloids

The ergot alkaloids, produced by Claviceps purpura, were the first

mycotoxins recognized to cause epidemic disease in humans. Persons who

ingested these mycotoxins, found primarily on moldy rye grain, developed

ergotism. A gangrenous form of ergotism was common in central Europe from

the 9th to the 14th century. 9, 10 The first symptom was a prickly sensation

in the limbs, which then became swollen, inflamed, and subject to sensations

of intense heat and cold. Peripheral vasoconstriction resulted in gangrene

and limb loss. In the Middle Ages, this was known as St. 's fire

because it was often cured by a visit to the shrine of St. , which

happened to be in an ergot-free region of France. A convulsive form of

ergotism involving the nervous system occurred in Europe from the late 16th

to the late 19th century. It was also reported in the United States and

historians have hypothesized that it may have been a factor in the Salem

witchcraft trials of 1692.11

The vasoconstrictive properties of ergot alkaloids have made them useful in

treating migraine headaches (ergotamine tartrate) and postpartum hemorrhage

(methyl ergonovine). Ergotism following ingestion of contaminated food is

very rare today; it is more commonly reported following therapeutic

administration of ergot alkaloids. 12, 13

Fumonisins

The fumonisins are a group of mycotoxins isolated from corn contaminated

with Fusarium moniliforme, F proliferatum, and A ochraceus. The fumonisins

were discovered in 1988 following the 1970 outbreak of equine

leukoencephalomalacia in South Africa. 14 Fumonisins seem to be universally

present in corn and corn-based products. 15 Extensive investigations have

documented that consumption of corn and corn-based products contaminated

with fumonisin B1 causes equine leukoencephalomalacia and porcine pulmonary

edema, fatal diseases in farm animals. 15 In 1989 and 1990, fatal outbreaks

of equine leukomalacia, porcine prenatal and neonatal mortality, and porcine

pulmonary edema occurred in the United States. 16-18 Evidence of human

health effects from ingestion of fumonisin-contaminated foods primarily

derives from studies in South Africa, China, and northern Italy. These

studies suggest a link between fumonisin exposure and esophageal cancer. 15

The fumonisins have been shown to disrupt sphingolipid metabolism. 19

Sphingolipids play a role in membrane and lipoprotein structure and in cell

regulation as second messengers for growth factors, differentiation factors,

and cytokines.19 Disruption of sphingolipid metabolism and its effect on

human development is under study.

Fumonisin exposure may play a role in birth defects. A 1990 cluster of

neural tube defects in south Texas generated the hypothesis that ingestion

of high levels of fumonisins in corn-based products might be linked to human

birth defects, such as anencephaly and spina bifida.20-23 Mexican Americans'

risks of neural tube defects are much higher than those of non-Hispanic

whites. 22 When the cluster of affected pregnancies occurred, US corn-based

products had relatively high levels of fumonisins, 2 to 3 times higher than

normal. Mexican American women in Texas, unlike their non-Hispanic

counterparts, eat a lot of corn in the form of tortillas (90 g/d vs 17

g/d).20 Fumonisin has been shown to interfere with cellular folate uptake 24

and it is possible that exposure to dietary fumonisins may help explain the

lack of effectiveness of folic acid in reducing neural tube defects in

Mexican Americans. 23

Trichothecenes

Fusarium and Stachybotrys species produce mycotoxins called Trichothecenes.

When ingested by humans, these mycotoxins produce alimentary toxic aleukia.

This disease first appeared in 1913 in far eastern Siberia 25 and was

reportedly responsible for the death of at least 100,000 Russian people

between 1942 and 1948. Affected persons developed necrotic ulcers in the

nose, mouth, throat, stomach, and intestines, complicated by hemorrhage from

the nose, mouth, gastrointestinal tract, and kidneys. Alimentary toxic

aleukia was associated with eating wheat and corn that had been under snow

during the winter and contaminated with Fusarium and Stachybotrys molds.

Dermal exposure to the Stachybotrys fungus may cause a severe skin reaction.

The dermatitis was first described among workers handling fodder, using

infected straw for fuel, or sleeping on mattresses made of infected straw

and is characterized by hyperemia, encrustations, and necrosis. 26

The acute toxicosis resulting from the inhalation of the Stachybotrys

mycotoxin, first described by Soviet scientists in the 1940s, has been

termed stachybotryotoxicosis. 27 The symptoms include sore throat, bloody

discharge from the nose, dyspnea, cough, low-grade fever, and chest

tightness.

Vomitoxin

Another trichothecene mycotoxin is deoxynivalenol, also known as vomitoxin,

frequently a contaminant of wheat and corn. In China from 1961 to 1985,

multiple outbreaks of vomiting illness were attributed to consumption of

vomitoxin-contaminated grain. 28 In India in 1987, nearly 100 persons became

ill after they consumed wheat products from which vomitoxin and other

trichothecene mycotoxins were recovered. 29 In 1997 to 1998, approximately

1700 US children became ill with vomiting, nausea, headache, and abdominal

cramps linked to eating burritos. 30 Although levels of vomitoxin in the

burritos were less than 1 ppm, the Food and Drug Administration (FDA)

advisory level, vomitoxin could not be eliminated as the causal agent

because this advisory level is set for adults and may not be applicable to

children. Ingestion of mycotoxin-contaminated food is the most important

route of exposure; 2 other routes should be recognized, as both dermal

absorption and inhalation of macrocyclic trichothecene mycotoxins have been

associated with human illnesses.

Satratoxin

Satratoxin is produced by Stachybotrys atra (also known as S chartarum).

This fungus can grow on any cellulose product in the presence of water.

Dissemination of spores into indoor air occurs when the fungus is disturbed.

An Epidemiologic study in 1994 found that 10 infants with life-threatening

acute pulmonary bleeding were more likely than a matched group of 30

comparison infants to live in homes with S atra and other molds in the air.

31 The findings linking S atra and other fungi to infant pulmonary

hemorrhage are controversial and have undergone careful scrutiny. 32-34

Additional research is needed to determine whether the reported association

between infant pulmonary hemorrhage and exposure to toxigenic S atra is

causal.

Exposure to S atra has subsequently been associated with acute pulmonary

hemorrhage in an infant in Kansas City, MO, 35 and with pulmonary

hemosiderosis in a 7-year-old in Houston, TX. 36 The Texas investigators

cultured S atra from the patient's bronchoalveolar fluid. Trichothecenes

suppress the immune system, leading to increased susceptibility to a variety

of infectious diseases. 37

Prevention

Both drought and flooding contribute to problems with mycotoxins. Fungi are

usually unable to penetrate intact seed kernels; drought may weaken the

plant, allowing penetration of the fungus. Mycotoxin problems in food may be

greater during years of extreme drought. 38 Intense rain and flooding can

also increase mycotoxin problems; intense rain events have increased by 20%

since 1900.39, 40

Massive contamination with mold is detectable and problems can be avoided by

not eating visibly moldy foods. The consumer cannot tell that processed

products have elevated levels of aflatoxins, vomitoxin, or fumonisins;

furthermore, these mycotoxins are not destroyed by heating. The FDA has set

action levels, informal nonbinding guidelines, for aflatoxins in food. The

FDA has advisory levels for vomitoxin but no established action levels and

has recently released a draft guidance document for industry on fumonisin

levels in human foods and animal feed. 41

Mycotoxins and Biological Warfare

One of the earliest uses of mycotoxins in warfare occurred in sixth century

BC when the Assyrians poisoned enemy wells with rye ergot. By the late

1990s, several countries had weaponized aflatoxin and there was suspicion

that Trichothecenes were also under investigation for use in biological

warfare. 42 Controversy exists about the purported use of T2 (a

trichothecene mycotoxin) in aerosol form (yellow rain) in Laos, Kampuchea,

and Afghanistan in the 1970s and 1980s. The only effective methods to

prevent exposure are physical protection of the skin and the airway;

treatment is limited to supportive care. Clinicians should be alert for

cases of unusual illness and report them to the local health department.

Historically, every discovery of the acute health effects of mycotoxins has

been prompted by reports of unusual illnesses from alert clinicians;

vigilance and early reporting are the most promising lines of defense

against the potential bioterrorist use of mycotoxins.

Author/Article Information

Author Affiliation: Division of Environmental and Occupational Health,

Washington University, School of Public Health and Health Services,

Washington, DC.

Corresponding Author and Reprints: Ruth A. Etzel, MD, Ph.D., US Public

Health Service, Alaska Native Medical Center, 4320 Diplomacy Dr, Anchorage,

AK 99508 (e-mail: retzel@...).

Contempo Updates Section Editor: Janet M. Torpy, MD, Fishbein Fellow.

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fumonisins.

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[Guest guest]

Date: Wed, 20 Jul 2005 23:10:58 -0700

From: <moldhelp@...>

Subject: stupid question on mycotoxins

I am a bit of a dunce here and I am not getting mycotoxins. I do know

however that they are produced in certain conditions and they are poisonous.

Could someone explain or point me to a website that explains HOW they are

toxic, what organs they attack, and what can be done to get rid of them

(besides avoidance). Maybe even symptoms ?

Thanks

Angelika

One other site of interest:

http://www.aces.edu/department/grain/ANR767.htm