Re: Interesting link - Innovative Aspects and Treatment of Molds, Mycotoxins and Che

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Branislav <arealis@...> wrote:

I've found an interesting article about the symposium on " Man and His

Environment in Health and Disease. Special Focus: Innovative Aspects

and Treatment of Molds, Mycotoxins and Chemical Sensitivity "

The whole text can be found at the following URL:

http://www.aehf.com/articles/2003Symp.htm

Here are some of the interesting excerpts from the text.

---------------------------------------

21st Annual International Symposium

on

Man and His Environment in Health and Disease

Special Focus

Innovative Aspects and Treatment of Molds, Mycotoxins and Chemical

Sensitivity

Sponsored by

American Environmental Health Foundation and

American Academy of Environmental Medicine

This activity has been planned and implemented in accordance with the

Essential Areas and policies of the Accreditation Council for

Continuing Medical Education (ACCME) through the joint sponsorship of

the American Academy of Environmental Medicine (AAEM) and the American

Environmental Health Foundation. The American Academy of

Environmental Medicine is accredited by the ACCME to provide

continuing medical education for physicians.

The American Academy of Environmental Medicine designates this

educational activity for a maximum of 21.5 hours in Category 1 credit

toward the AMA Physician=s Recognition Award. Each physician should

claim only those hours of credit that he/she actually spent in the

activity.

Reprints are available from American Environmental Health Foundation.

This volume is not to be reproduced, all or in part, without the

written permission of American Environmental Health Foundation.

INTRODUCTION

SYMPOSIUM PURPOSE

Since 1981, the International Symposium has been recognized as one of

the most advanced medical forums in the world addressing the research

and treatment of environmental effects on health and disease. The

2003 conference will focus on " Innovative Aspects and Treatment of

Molds, Mycotoxins and Chemical Sensitivity " . For this year=s

conference, we have assembled a faculty of top international experts

for you. This Conference presents the most current information

available while providing guidelines to identify, diagnose, treat and

to prevent environmentally triggered responses in the body.

GOALS OF THE MEETING

! To provide new insights into the mechanisms and

the environmental causes behind many problems you see.

! To present new diagnostic and treatment

modalities to help you improve the quality of care for your complex

patients.

! To provide concepts, tools that will enhance your

practice.

OBJECTIVES OF THE MEETING

! Improve the outcome of treating patients with

chronic disease, nutritional problems and chemical sensitivity.

! Use new concepts and treatments to help better

diagnose and manage many patients with chronic disease, nutritional

problems and chemical sensitivity.

! Apply the concepts of this conference to your

practice by using nutrition and environmental manipulation for the

treatment of chronic disease, nutritional problems and chemical

sensitivity.

! Use the information presented to enhance the

effectiveness, cost-efficiency, and competitiveness of your practice

in relation to chronic disease, nutritional problems and chemical

sensitivity.

INTENDED AUDIENCE

M.D.=s, D.O.=s, D.D.S.=s, medical students, nurses, nutritionist, and

all other health professionals interested in the concepts and practice

of Environmental Medicine, Occupational Medicine and Toxicology.

EDUCATIONAL FORMATS

# Plenary

# Panels Discussions

# Case Studies

# Question & Answer Sessions.

CONFERENCE FORMAT

The AEHF Committee has selected some of the leading experts in the

fields of chronic disease, nutrition and chemical sensitivity.

Each speaker=s presentation will last approximately 20 minutes and

will be followed by a 10 minute question and answer session. All

speakers are encouraged to use any and all appropriate audio/visual

aids. (A brief outline of the speech is included in this booklet.)

GIVEN IN COOPERATION

J. Rea, M.D., F.A.C.S.

Symposium Chairman,

American Environmental Health Foundation,

Environmental Health Center - Dallas,

Dallas, Texas

Bertie B. Griffiths, Ph.D.,

Environmental Health Center - Dallas

Dallas, Texas

Kaye H. Kilburn, M. D.

University of Southern California Medical Center

Keck School of Medicine

Los Angeles, CA

J. Meggs, M.D.

Dept. of Emergency Medicine

E. Carolina Univ. School of Medicine

Greenville, NC

Allan D. Lieberman, M.D.

Center for Occupational Environmental Medicine

North ton, SC

Mycotoxins in Indoor Climates

Tapani Tuomi

As of present, analyzing for mycotoxins in indoor environments is

difficult, if the goal is to assess the health consequences of

extensive water damage on the occupants of a particular building.

There is accumulating evidence on the presence of mycotoxins in crude

building materials1-7 as well as a body of indirect evidence linking

the presence of mycotoxins in indoor environments to health problems5,

8-15. It is frequently maintained that mycotoxins present in bulk

materials infested with toxigenic fungi are carried to indoor air by

fungal propagules. It follows that the route of exposure to mycotoxins

in indoor environments is inhaling dust particles containing toxigenic

fungal propagules2.

Dose-responses of humans to airborne mycotoxins are not known and it

seems that mycotoxin concentrations in inhalable dust would have to be

some 100-fold higher than what is frequently encountered in indoor

environments for air sampling to be feasible on a general level. If

air sampling is not attempted, deposited dust constitutes one step

closer to the composition of indoor air with respect to mycotoxins.

There are numerous studies from agricultural environments establishing

that mycotoxins present in bulk material are - given the right

circumstances - carried into dust. For instance, trichothecene

concentrations of 0,1-1 µg/g dust, aflatoxin concentrations of 0,02-5

µg/g dust, ochratoxin A concentrations of 0,2-70 ng/g dust, and

zearalenone concentrations of 20-100 ng/g dust have been reported

during grain handling and from other agricultural settings16-21. In

laboratory settings, Sorensen et al.22 found satratoxin concentrations

in the 10 µg/g dust-range, whereas Smoragiewicz et al.6 detected

trichothecenes in deposited dust from a moisture problem building in

amounts exceeding 0.4-4 µg/g and Engelhart et al.23 found

sterigmatocystin (2-4 ng/g) in carpet dust from a damp indoor

environment. It follows that samples of deposited dust should be

considered alongside with bulk samples when assessing the presence of

mycotoxins in indoor environments.

In agricultural settings, aflatoxin concentrations of 0,01 - 1000

ng/m3 and eoxynivalenol (DON) concentrations of 3-20 ng/m3 have been

reported in air17-18, 20-21, 24-25. In indoor environments, satratoxin

in concentrations of 0,1-0,5 ng/m3 and unidentified trichothecenes in

concentrations of 1-35 ng/m3 have been found22-23. It seems therefore,

that irrespectively of the environmental setting, whether agricultural

or indoor environments, measurement of airborne mycotoxins generally

require use of high-volume samplers in combination with sensitive

chemical or immunological methods of analysis. Risk-assessment on the

inhalation of mycotoxins cannot be made based on the analysis of bulk

samples of construction materials. Neither can mycotoxin contents of

deposited dust serve as basis of risk-assessment. Therefore, with the

development of more efficient methods of sampling and analysis, air

sampling will help us better understand the health consequences of

exposure to mycotoxins in indoor climates and perhaps will at some

point enable estimation of dose-responses of humans to airborne

mycotoxins.

In conclusion, a wide range of mycotoxins are potentially present in

indoor climates harboring moldy surfaces. It has proven difficult,

however, to establish the presence of mycotoxins in indoor air. This

does not take away from the fact, however, that mycotoxins may

contribute to the variety of symptoms experienced by patients exposed

to moldy propagules in indoor climates.

REFERENCES: 1Andersson et al., Appl Environ Microbiol, 1997, 63:

387-393; 2Croft et al., Mycopathologia, 1986, 151:93-98; 3Flappan et

al., Environ Health Perspect, 1999, 107: 927-930; 4Gravesen et al.,

Environ Health Perspect, 1999, 107: 505-508; 5Johanning et al., Int

Arch Occup Environ Health, 1996, 68: 207-218; 6Smoragiewicz et al.,

Int Arch Occup Environ Health, 1993, 65: 113-7; 7Tuomi et al., Appl

Environ Microbiol, 2000, 66, 1899-1904; 8 Auger et al., Am J Ind Med,

1994, 25: 41-2; 9Hodgson et al., J

Occup Environ Med, 1998, 40: 241-9; 10, Atm Environ, 1992, 26A:

2163-2172; 11Morb Mortal Wkly Rep, 1994, 43: 881-883; 12Morb Mortal

Wkly Rep, 1995, 44: 67-74; 13Morb Mortal Wkly Rep, 1997, 46: 33-35;

14Rautiala et al., Am Ind Hyg Assoc J, 1996, 57: 279-84; 15 et

al., Fems Microbiol Lett, 1992, 79:337-43; 16 Lappalainen et al.,

Atmosph Environ, 1996, 30, 3059-3065; 17Burg et al., Am Ind Hyg Assoc

J, 1981, 42:1-11; 18Burg et al., Am Ind Hyg Assoc J, 1982, 43:580-587;

19Silas et al., Am Ind Hyg Assoc J, 1987, 48:198-201; 20Selim et al.,

Am Ind Hyg Assoc J, 1998, 42:252-256; 21Palmgren et al., Am Ind Hyg

Assoc J, 1983, 44:485-488; 22Sorenson et al., Appl Environ Microbiol,

1987, 53: 1370-5; 23Engelhart et al., Appl Environ Microbiol, 2002,

68:3886-3890; 24Ghosh et al., Am Ind Hyg Assoc J, 1997, 58:583-586;

25Kussak, Ph.D. Thesis, Umeå University, Umeå, Sweden, 1995.

22Johanning et al., Unpublished data pertaining to filter no. 1 in

Johanning et al., Proceedings: Indoor air 2002; 23Yike et al., Appl

Environ Microbiol, 1999, 65: 88-94.

Immunological and Neurophysiological Abnormalities in Adults with

Exposure to Molds

W. , M.D.

High, M.D., Ph.D.

Ebere Anyanwu, M.S., Ph.D.

Medical Center for Immune and Toxic Disorders

Houston, Texas

Objective: The objective of this study was to evaluate the

immunological and neurophysiological effects in patients (378) who

presented to our medical center with various adverse health problems

due to documented exposure to indoor toxigenic molds. Exposure to

indoor toxigenic molds and the subsequent effects on humans is ranked

high among environmentally related disorders. Recently, occupational

exposures in nonagricultural settings have been investigated using

modern immunological laboratory tests. Few studies exist that take

into account the combined immunological and neurophysiologic effects

in humans.

Methods: We studied retrospectively patients with documented

toxigenic mold exposure at measured levels in their residence using

previous medical records, questionnaires, serum testing for antibodies

to molds, serum immune function testing and neurophysiological testing

including electroencephalogram (E.E.G.), brainstem auditory evoked

response (B.A.E.R.), visual evoked potentials (VEP), and nerve

conduction velocity (NCV).

Results: Findings from indoor environmental studies on the patients'

residence (exposure site) were positive for specific levels of

exposure to toxigenic molds including Penicillium, Aspergillus,

Fusarium, Chaetomium, and Stachybotrys species. There was a positive

correlation between findings from the neurophysiological and

immunological studies and the exposure to indoor molds found in the

residence. The objective immunological and neurophysiological

findings were significantly abnormal, indicating both immunotoxic and

neurotoxic effects.

Conclusions: A statistically significant number of patients with

known chronic exposure to toxigenic molds developed immunologic and

neurophysiologic abnormalities. Our findings revealed the extent to

which toxigenic molds can affect the immunological and neurological

systems of environmentally exposed individuals. Further work is

encouraged in this regard.

-----The Pathology of Trichothecene Mycotoxicosis In Humans-------

1. The Fingerprint of the Agent Causing the Disease is Displayed

Within the Cells or Tissue of The Body.

2. Degeneration and Necrosis of The Entire Central Nervous

System, Cardiovascular, lung, Digestive Tract, Spleen, Liver, Kidney,

Pancreas, Immune, Skin, Reproductive, Eye, Urinary Bladder and Prostate.

3. The Signs and Symptoms Described For Trichothecene

Mycotoxicosis Match the Pathology Observed.

4. Every Cell in The Body is Affected or Susceptible to

Trichothecene Mycotoxins When Exposed.

5. The Exposed Cells Are Not Allowed to Grow and Make Cellular

Products in The Rough Endoplasm Reticulum Represents of First

Mechanism of Action on The Cells.

6. The Burning or Denaturation of Tissue From the Epoxide

Molecule is Another Mechanism of Action on The Cells of The Body

Causing Intense Scarring of Organs. (Like Phenol)

7. The Rapidly Turnover Organs Systems Are Affected The Most

Severe, G.I. Tract, Immune System and Reproductive, (like radiation

damage)

8. The Central Nervous System is Severely Affected and is A

Primary Target Organ. The Neurons in the Cerebral Hemispheres, White

and Grey Matter, Brain Stem and even the Ependymal Cells. The

Purkinje Cells of The Cerebellum Are Severely Affected That Affect

Motion and Balance. The Dorsal and Ventral Motor Neurons Are Destroyed

Causing Amyotrophic Lateral Sclerosis. Peroxidation of Peripheral

Nerves is Also Observed. The Central Nervous System is The Organ Most

Affected as Reported By People Exposed to Toxic Mold.

9. Lack of Cellular Production, Epoxide- Peroxidation of Lipid

Membranes, Loss of Vessels, Loss of Oxygen From Severe Lung Scarring,

and Loss of Proper Nutrients Due Loss of Functional Absorption of

Intestine Affect the Brain and All Organs of The Body.

10. The Trichothecene Mycotoxins are Cumulative in Their Health

Effects on Organ Systems.

11. Trichothecene Mycotoxins are " Hit and Run " Poisons and are not

Stored in The Body.

12. Inhalation of Trichothecene Mycotoxins Are More Poisonous As

Observed by The Intense Scarring of The Alveolar Tissue Than

Consumption Due To The Neutralization of Mycotoxin by Bacteria.

13. Depression of the Immune System Allows for Increase Infections

by Bacteria, Viral, Fungal and Cancer to Form.

14. Yeasts are allowed to Colonize the Intestine Tract Because They

Are Resistant to Trichothecene Mycotoxins.

15. Yeast Can Cause Diabetes Mellitus, Gout and Prevent Proper

Liver Function to Detoxify Xenobiotics.

16. Trichothecene Mycotoxins are Released Within the Urine and

Feces as Evidenced by The Pathology Observed Within Those Tissues.

17. Children Exposed to Trichothecene Mycotoxins are 100 to 1000 X

more susceptible because stems are killed not allowing for additional

growth within the individual.

18. There is No Safe Level of Exposure to Trichothecene Mycotoxins.

19. The third Mechanism For Trichothecene Mycotoxicosis is To

Develop Anaphylaxis to Mold Allergens When Mycotoxin Leaves The Body.

Dr. Croft, (Medical Pathologist)

Stages of Mycotoxicosis: For Inhalation of Mycotoxin

The three Stages (1-3) ranging from lower to higher severity of

poisoning were modified according to exposure via the air as opposed

to ingestion already established (Forgacs et al., 1962; Joffe, 1971).

A separate Stage of convalescence occurs when a patient is completely

removed from the contaminated premises and the source of mycotoxin or

mold spores.

Stage 1: The primary changes are in the brain, respiratory and immune

systems, mucus membranes and gastrointestinal tract. Signs and

symptoms may include burning sensation in the mouth, tongue, throat,

palate, esophagus, and stomach, which is a result of the action of the

toxin on the mucous membranes and skin in the exposed areas. Moist

areas of the body armpits, under breasts, belt line and groin are more

sensitive or first affected. Patients may report burning within the

eyes, ears and nose. Patients also reported that their tongues felt

swollen and stiff. Mucosa of the oral cavity may be hyperemic. Mild

gingivitis, stomatitis, glositis, and esophagitis developed.

Inflammation, in addition to gastric and (small and large) intestinal

mucosal, resulted in vomiting, diarrhea and abdominal pain. Excessive

salivation, headache, dizziness, weakness, fatigue and tachycardia

were also present.

There may be fever and sweating. The respiratory system develops

burning sensations and congestion. Severe exposure to mycotoxin within

the lungs may lead to congestion, edema and failure, due to caustic

action. Body temperature remains normal and controllable by the

patient. The poisoning appears and disappears relatively quickly in

this Stage with the exception of, lungs and central nervous system.

Initially (Stage 1), the patient's symptoms are very uncomfortable or

painful. As the poisoning continues and the patient progress toward

Stage 2, he or she becomes accustomed to the presence of the mycotoxin

and a quiescent period follows due to lack of nerve sensation.

Depending on exposure levels, the first Stage may last from 3 - 9

days. In scoring the 50 signs and symptoms listed in Tables-1 and 2,

an average score range of 20-45 represents Stage 1.

Stage 2 : This Stage is often called the latent Stage or incubation

period because the patient feels apprehensive, but is capable of

normal activity in the beginning of this Stage. Every organ of the

body is affected by degeneration and necrosis with continued exposure.

The primary target organs for an individual become evident over time,

due to biological variation. These are disturbances in the central and

autonomic nervous systems resulting in headaches, mental depression,

loss of short-term memory, loss of problem-solving ability, various

neuropsychiatric manifestations, meningism, severe malaise and

fatigue, narcolepsy, loss of temperature control, hyperesthesia or

numbness of body areas, and cerebellar dysfunction including

hypotonia, attitude and gait, dysmetria, asthenia, vertigo,

disturbances of speech, and loss of balance (Best, 1961). Spinal cord

degeneration may also be observed in gait and reflex abnormalities,

such as the ability to drive vehicles, ride bicycles or pass sobriety

tests (inability to tolerate ethyl alcohol). Attention deficient

disorder may be observed in children. Various systems may include:

Eyes: visual disturbances, floating objects, light sensitive, lack of

tears, burning and itching. Ears: burning, itching, and loss of

hearing. Immune and hematopoietic: progressive loss of white and red

cells including a decrease of platelets and hemoglobin, and high

susceptibility to bacterial, mycotic and viral infections,

debilitating chemical and allergies. Gastrointestinal: metallic taste

in mouth, tooth loss, gum problems, stomatitis, sores in gums and

throat, nausea, vomiting, diarrhea or constipation, excessive

flatulence, abdominal distention, hepatitis, pancreatitis, and

diabetes mellitus. Respiratory : burning and bleeding from nasal

membranes, respiratory difficulty, asthma, extreme susceptibility to

cold, flu and pneumonia. Skin: thinning of hair on head, burning on

face, rashes, irritation, and edema. Renal: proteinuria, possible

hematuria. Reproductive: irregular ovarian cycles, increased menstrual

flow, fibroid growths in uterus, cystic development in mammary glands,

and tumors of mammary and prostate glands. Musculoskeletal :

somatitis, muscle weakness, spasms, cramps, joint pain, enlargement of

joints in hand, and clubbing of fingers. Cardiovascular: chest pain,

palpitations, ruptures of atrial walls, myocardial infection and

aneurysm of arteries.

The skin and mucous membranes may be icteric, pupils dilated, the

pulse soft and labile, and blood pressure may decrease or increase.

The body temperature does not exceed 38 degree C and the patient may

be afebrile, or chilled. Visible hemorrhagic spots may appear on the

skin. Thoughts of suicide may be prominent in the person's mind at

this time or anytime in Stage 2. Human bonding is very important for

survival.

Degeneration and hemorrhages of the vessels marks the transition from

the second to the third Stage of the disease and may not be

consistently observed. The degeneration of the vital organs including

serious respiratory insufficiency or asthma and CNS degeneration will

take the patient into Stage three along with development of necrotic

angina. If exposure continues, depending on exposure levels, Stage 2

may continue from weeks to months or even years until the symptoms of

the third Stage develop. Evaluating the 50 signs and symptoms (Table-1

and 2) by assigning a score (0-least intense to 5-most intense or

severe) to each symptom, we have determined that an average score

range of 45-180 represents Stage 2.

Stage 3: Severe degeneration of the vital organs. The transition from

the second to the third Stage is sudden. In this Stage, the patient's

resistance is already low, and violent severe symptoms are present,

especially under the influence of stress, or associated with physical

exertion and fatigue. The first visible sign of this Stage may be

lung, brain or heart failure (heart attack), with or without the

appearance of petechial hemorrhage on the skin of the trunk, the

axillary and inguinal areas, the lateral surfaces of the arms and

thighs, the face and head, and in serious Cases, the chest. The

petechial hemorrhages vary from a few millimeters to a few centimeters

in diameter. There is increased capillary fragility and any slight

trauma may cause the hemorrhages to increase in size.

Aneurysms of the brain or aorta may be observed by angiography.

Hemorrhages may also be found on the mucous membranes of the mouth and

tongue, and on the soft palate and tonsils. There may be severe

interstitial thickening or scarring of the lungs, or respiratory

failure. Nasal, gastric and intestinal hemorrhages and hemorrhagic

diathesis may occur. Necrotic angina begins in the form of catarrhal

symptoms and necrotic changes soon appear in the mouth, throat, and

esophagus with difficulty and pain on swallowing. Severe degeneration

of the skin on the face, eyelids, and loss of lashes is also often

present.

Necrotic lesions may extend to the uvula, gums, buccal mucosa, larynx,

vocal cords, lungs, stomach, and intestines and other internal organs

such as the liver and kidneys and are usually contaminated with a

variety of avirulent bacteria. Bacteria infection causes an unpleasant

odor from the mouth due to the enzymatic activity of bacteria on

proteins. Areas of necrosis may also appear on the lips and on the

skin of the fingers, nose, jaws, and eyes. Regional lymph nodes are

frequently enlarged. Esophageal lesions may occur and involvement of

the epiglottis may cause laryngeal edema and aphonia (loss of voice).

Death may occur by strangulation.

Patients may suffer an acute parenchymatous hepatitis accompanied by

jaundice. Bronchopneumonia, pulmonary hemorrhages, and lung abscesses

are frequent complications. Tumors may develop of various organs,

including skin, urinary bladder, brain, mammary gland, bone, immune,

liver, prostate, possibly resulting in death. The most common cause of

death is brain failure due to both direct effects of the mycotoxin on

the central nervous system and indirect effects due to respiratory

failure or lack of oxygen to the brain caused by the severe caustic

inflammation (fibrinous exudation) reaction with the lung tissue,

rendering it non-functional. Again, using the scoring system

represented in Tables-1 and 2, an average score of greater or equal

180 represents Stage 3.

Stage of Convalescence: The course and duration of this Stage 3

depends on the intensity of the poisoning and complete removal of the

patient from the premises or source of mycotoxin. Therefore, the

duration of the recovery period is variable. There is considerable

cellular necrosis and scarring to all major organs of the body in

which cells will not regenerate, including the brain, spinal cord,

eyes, lung, heart, liver, pancreas, kidney, adrenal, and blood

vessels. If the disease is diagnosed during the first Stage,

hospitalization is usually unnecessary, but allergies and asthma

should be monitored closely. If the disease is diagnosed during the

second Stage and even at the transition from the second to third

Stages, early hospitalization may preserve the patient's life. If

however, the disease is only detected during the third Stage, death

cannot be prevented in most Cases.

1. Croft, W. A., Jastromski, B. M., Croft, A. L., and s, H. A.,

" Clinical

Confirmation of Trichothecene Mycotoxicosis in Patients Urine " ,

In: Journal of

Environmental Biology 23(3), 301-320 (2002)

2. .Forgacs, J., and W. T. Carll : Mycotoxicoses. In : Advances in

Veterinary

Science. Academic Press, New York and London, pp 273-372 (1962).

How Molds and Mycotoxins Affect Human Brains

Kaye H. Kilburn, M.D.

University of Southern California, Keck School of Medicine

Background: Mold spores and mycotoxins produce airway irritation,

asthma and bleeding. Neurobehavioral and respiratory symptoms

suggested testing.

Methods: Neurobehavioral functions as means of percent predicted were

compared in 65 consecutive mold exposed adults and 202 community

controls. Measurements included balance, choice reaction time, color

discrimination, blink reflex, visual fields, grip, hearing, problem

solving, verbal recall, perceptual motor speed, and memory. Check

lists surveyed histories, mood states and symptom frequencies (Kilburn

2002a and 2002b).

Findings: Exposed persons had abnormal balance, reaction time, blink

reflex latency, color discrimination, visual fields, and grip. Also

digit symbol substitution, peg-placement, trail making, verbal recall,

and picture completion scores were reduced. Twenty-one of 26 tested

functions were abnormal. Airways were obstructed and vital capacities

reduced. Mood scores and symptom frequencies were elevated.

Interpretation: Mold exposures indoors were associated with

neurobehavioral impairment probably from mycotoxins, such as

trichothecenes. Correlation of human impairment with measured

mycotoxins is the next step (Johanning et all 1999 and 2002, Nielsen

and Thrane 2001).

REFERENCES

1. Kilburn KH. Janus Revisted, Molds Again. Arch Environ

Health 2002a;57(1):7-8.

2. Kilburn KH. Inhalation of Moulds and Mycotoxins. Eur J

Oncol 2002b;7(3):____.

3. Johanning E et al. Clinical Experience and Results of a

Sentinel Health Investigation Related to Indoor Fungal Exposure.

Environ Health Perspect 1999;107(3):489-494.

4. Johanning et al. Airborne Mycotoxin Sampling and Screening

of Trichothecenes in Fungal Cultures - Using Gas Chromatography -

Tandem Mass Spectrometry. J Chromatography A 2002;929(1):75-87.

---------------------------------

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[Guest guest]

Thanks Branislav for this. Great find and very informative!

Dana

> I've found an interesting article about the symposium

on " Man and His

> Environment in Health and Disease. Special Focus: Innovative

Aspects

> and Treatment of Molds, Mycotoxins and Chemical Sensitivity "

>

> The whole text can be found at the following URL:

>

> http://www.aehf.com/articles/2003Symp.htm

>

>

>

>

>

>

>

> ---------------------------------

> Looking for earth-friendly autos?

> Browse Top Cars by " Green Rating " at Autos' Green Center.

>

>