Transcript and video from the Dec 6 NTP meeting Mold. Shoemaker & Hudnell

[Guest guest]

Hi All,

The transcript and video from the Dec 6 NTP meeting in which the need for

further study into the toxicological properties of indoor mold exposure was

discussed is now available.

_http://ntp.niehs.nih.gov/index.cfm?objectid=1C10B753-F1F6-975E-7E6D41437E9A8F

33_

(http://ntp.niehs.nih.gov/index.cfm?objectid=1C10B753-F1F6-975E-7E6D41437E9A8F33\

)

I have just skimmed this, but I pulled out the Hudnell/Shoemaker testimonies.

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.

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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At least initially we will not look, but there has been suggestions to do

these in reproductive and in developmental studies, a good potential candidate

for per I natal studies, those type, per I natal exposure, neuro, immuno

toxicity, and reproductive and developmental issues. One of the issues in terms

of developing the next tier of studies is we need more guidance on what to

study. We won't be able to look at all of the mixtures, individual components

in

these types of studies. That's a life-time research study for me. I think we

are trying to focus a little bit on the hazards identification aspects at

this point, and then we will move on to the more specialized focused types of

studies.

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