NTP Dec.6th meeting now available. Need for study of mold toxicity

[Guest guest]

Wed Jan 2, 2008 1:29 pm

snk1955@...

I wanted to let you all know that the NIEHS National Toxicology

Program meeting of Dec 6, 2007 is now available in pdf form and on

video. One can read it/view it at the following link. There is

much discussion of the victims of Katrina within this meeting and

the need to better understand the illnesses they are experiencing

from mold exposure, far beyond simple allergic reactions. This is a

great step in the right direction that will help many!

http://ntp.niehs.nih.gov/index.cfm?objectid=1C10B753-F1F6-975E-

7E6D41437E9A8F33

In case someone does not want to take the time to rummage thru the

entire meeting, I pulled out Dr. Ken Hudnell's testimony and Dr.

Shoemaker's testimony. Between the two, it gives a good overview of

the gist of the matter. (be forewarned, the typos are numerous in

the transcript)

WR,

Sharon

Dr. Germolec:

" We are using a mixture of mold and will be obtaining a culture from

a house that was saturated during Hurricane Katrina. So what we hope

to provide information then would be on exposures to make shoes of

organisms that might be commonly found in homes falling in the event

like Hurricane Katrina. "

Dr. Hudnell:

Good morning. I am very grateful to have the opportunity to address

the NTP this morning on the topic of mold and human health. I

commend you for taking on the role, there's long been a need for

leadership on the area, very slow coming. Hasn't come from CDC, from

EPA, you just heard how they are looking at A jerjic aspects of

mold, allergic, but it's important to look at the toxic aspects of

mold. I have been a neuro toxicologist for 23 years at EPA studying

human health effects related to a variety of compound exposure, air

borne metals, pesticides, and the last 10 years I have focused on

mold or biotoxin associated illness.

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Most recently I led an interagency effort to address the issue --

single cell organisms that make multipole and highly ponent toxins,

much like mold does here. I have addressed reports on that issue,

and the editor, coauthor of a 1000 page book about to come out on

the -- state of the science and research needs. I am glad to be able

to address you today about mold, you can see I am pretty excited

about having left EPA, Tuesday was my last day at EPA, have now

joined a company that the best solution to fresh-water blooms.

Before I address the risk management aspect of clinical

intervention, now addressing the risk management aspect of

preventing molds.

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I want to make a few brief points, leading to what we call biotoxin -

- a contentious area, as you have heard, inappropriate position

papers misleading the public. This problem will ultimately be

resolved when someone like the NTP takes leadership, and was so well

expressed today in earlier talks, will combine what can be learned

from human and animal research.

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It's a highly-complex mixture to which humans are exposed when in

water-damaged buildings. Many types, as well as fragments released

to air and humans breathe in a very complex mixture that can

involve, if you if you various compounds, and toxins. This is an

example that it's important to do what you are doing, look at

mixtures. This is not a simple -- this paper gives example, one if

you think fungi, one -- fungi, one -- a variety of mechanisms to

which they -- they often verge on one common pathway, the induction

of an inflammatory response, primarily governed by the immune system.

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So, with Dr. Schumacher and others, I looked at illness for a long

time, starting with fister ya, and human mold illness, we have --

bacteria, Lyme disease, a toxic illness that follows the disruption

of the bacteria. Biotoxin-associated illness is very frequent

characterized by a variety of symptoms, due largely to inflammatory

responses being initiated, can vary in people from day-to-day. We

found a useful indicator of neurological effects by looking at

visual contrast sensitivity; a process through which visual patterns

are detected. We found in biotoxin-associated illness, a large,

maybe 60% loss of ability to detect patterns, and we can see

recovery of this, along with symptom abatement when we treat people

with coul owe stire owe mean, a compound that vastly increases toxin

elimination rates. I encourage you to think about using some of this

intervention aspects in your studies, the coul owe sire owe mean is

shown to vastly increase the elimination rate of a wide variety of

toxic ins, including some micro toxins.

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Some of the main things we see in -- the abnormalities of the --

pathway, increases in -- probably due to damage to -- receptors, and

the result of low levels of MSH, markers of damage, all coming about

due to inflammation caused by cytokines, and the -- complement

factors.

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As we mentioned, it's a contentious area. I was really shocked when

the ACOM came out with a position paper authored by a few people

that basically reached what they claimed to be a definitive

conclusion, that it's highly unlikely that humans are ever going to

get sick from this complex mixture of things found in water-damaged

buildings. What did they base this on? One single mouse study,

exposed three weeks to one stipe type of spore. They also used

literature showing this level at which effects were seen is unlikely

to be found in indoor air because they looked at a survey of

building concentrations of mold in buildings where people weren't

sick.

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They really failed to address a lot of issues. This study did not

show -- other studies indicated the Noelle is quite a bit lower than

the level their study had. They failed to realize that people aren't

just exposed to spores, but there are many times more fragments,

loaded with toxic substances that people were exposed to when they

inhaled air in these buildings. They tested the least susceptible

population in this rodent study. Three weeks of exposure doesn't

come close to what human experience. Most humans get sick after

months of exposure.

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Most shocking to me is that you make, they would make a statement on

human health risk assessment without doing a risk assessment. There

was no taking into being the account all the things -- no

susceptible populations, short-term rather than chronic exposure, no

information on developmental effects, cars no gistity, disregarding

the need for need assessment.

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You have two minutes remaining.

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As we said, it's a very complex mixture. The NTP has the tune the to

opportunity to really take a leadership role by partnering with

people to do the human research, do complementary work together with

NIEHS or together with -- that's it, thank you very much.

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Thank you, express our thanks to Mrs. Kramer.

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Next speaker is Shumacher.

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Good morning. I thank you for the opportunity to talk to you about

my passion. I've been a private practice physician for many years,

practice started in 97 where blooms of an organism, fister ya, made

people ill, and there was no one to help me with what to do, how to

evaluate patients with s with these illnesses. I I am pleased to

here the NTP recognizes the number of illnesses that need to be

evaluated and specifickyally the roster of organisms ever

increasing. I wouldn't have last year put micro bacteria on the

list, now I will. Proteins made by stacky boit rise, excellent paper

from Dr. Dearborn, hem a lice ins, materials inflam owe Jens

identified identified in -- found in organism and buildings. These

are real, we know them now. I don't know what the list will be next

year. I would emphasize the spore counting is, in my opinion, now,

not a very useful exercise. Focusing on spores ignores the very

large part of the iceberg.

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Specifically, I have over 4500 patients in Excel data sets I have

looked at over the years. We know there's a very strong genetic

basis to the illness. 40% of the population will have -- associated

with the increased relative riff being in illness acquisition. That

means 76% don't. A sick patient and non-sick, with the same exposure

need to be looked at, and separating cases in controls when looking

at genetic aspects. We know full well if we follow not acquired

immunity, cases are no different than I GE controls. I hear you

focusing on I GE, that has merit, but not the same as focusing on

innate immune elements. The final pathway of deficiency --

critically important. I hope the FDA guy will help me figure out how

to get exemption, they are all deficient, all needed. Specifically

what we have done in my office, take patients who willingly need to

know if a given environment makes them sick. They come in ill,

fortunately we can treat them, reduce the very many biomarkers we

control, stop interventions, let them go to other environments other

than potentially water-damaged buildings we think might be making

them sick, we document, no change in symptoms. Put them back in the

affected building, measure biomarkers on day one, two, three. That

ability to see prospective change of illness presentation without

any other confounders in time gives us a chance to assess causation.

Also gives a chance to create a health index -- innate immune --

that's all on the printed material. Specifically treatment, not the

focus of your discussion today, but I will tell you coul owe stire

owe mean is your first step. We need to look at these very unusual

bio-- deep nasal spaces, hardly ever found in controls, these

organisms make toxins that cleave -- and must be removed to have

treatment follow. Must be down-regulated, comment about

abnormalities and -- T-cell abnormalities are common, and these

patients in children especially compared to adults, 58% of kids will

have -- antibodies without cell ciliac disease -- walking around

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A huge issue, we worry about angiogenesis, cancer, most have

incredibly low veg F, we look at the feck by -- see the delivery of

oxygen is down in the range of class 3 and 4 heart failure in these

patients. The toxins, activation are hugely important, C 4 A is

probably the most important marker we look now. We published a paper

and have one coming forward.

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You have two minutes.

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The cognitive issues have dominated my practice the last half year.

Where do these come from? We are doing -- in patients with a 1.5

tees la coil in Salisbury and can show in cases compared to controls

extremely high elevated levels of lactate compared to glutamate,

ratios, high levels of C 4 A and many coggingative symptoms. We

selectively treat for high C 4 A, not enough to make clotting occur,

we see symptoms disappear, resolution of lactate elevation and

normalization of --

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We don't know if -- is so important why do these illnesses appear

only after a -- event. Is there an effective antigen presentation .d

recovery, made ill again, markers higher -- you do animal study and -

-

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Looking at the role of innate and immune receptors, we need -- in

these patients, and the role of bleeding is well explained with

acquired -- disease.

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Specifically we don't know if HLA is the same in rats and mice and

men. Must look for , absence of -- in patients. It's incredibly

important. I have not seen any good studies. Be nice to find --

specific assay with no NOAA, looking at -- inflammatory genes

analyzed, hoped to have ready for today, presentation out next week,

research is encouraging looking at the behave being mechanism of

illness. The real issue I want to leave you with is that there's a

pathway in a model for illness acquisition in people that is seen

reproducibly. Each of the elements that are abnormal here contribute

to the illness and each must be addressed to achieve wellness.

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Thank you for your comments and written materials. I will turn back

to the board for questions of the speakers or of Dr.

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Dr. ?

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I would like to make one comment. First impression might be this is

a problem that's common in areas of moist environment like the

southeast or northwest. I would like to point out the state of New

Mexico is in the top 10 states where you find production of molds,

in spite of the fact we have 8 to 10 inches of rain a year. We get a

little moisture and the molds go nuts. If you have a building where

you have a water leak, if it rains you have all this mold that

enters the air, fragments, microbe rail fragments, spores, buildings

in Albuquerque where we have toxic mold problems.

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Thank you. I had another question about the design. You mentioned

New Mexico's problem, should be recognized hospitals have a problem.

Our unit, premature babies, we just had a mold event. Had you

looking to characterizing extremely early life exposures. From the

model, this probably will not capture that population.

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