Re: Endotoxemia/Endotoxicosis from Water Damaged Buildings

[Guest guest]

--- In , LiveSimply <quackadillian@...>

wrote:

>

> I've noticed that there is quite a bit of science on endotoxin

exposure, and

> that endotoxin levels are quite high in water damaged buildings,

> particularly ones that involve flooding or similar.

>

> Why doesn't this get brought up more? Its obvious to me that it

matters

> substantially.

>

> Clean dry buildings don't have these high endotoxin levels, water

damaged

> buildings do.

I totally agree with you. When one gets sick in a damp building,

there is ususlly a unique " cocktail " of exposure which includes

fungi, bacteria and yeasts. As far as I am concerned, it is the mix

that makes you sick.

[Guest guest]

Exactly!

This synergism seems increasingly as if it might be really important!

A growing body of research is documenting a substantial (more than

ten-fold, sometimes mouch more) increase in the toxicity of a number

of mycotoxins when the exposure is contemporaneous or was immediately

preceded by an exposure to endotoxin. Given that endotoxin exposure to

humans is COMMON, IMO this synergism is clearly an important factor in

water damaged building toxicity. There are lots of papers showing how

this mechanism works.. its not just mycotoxins that are " primed " -

this mechanism is also involved in creating hypersensitization..

The Endotoxin part of the pre-exposure can apparently come from

inhalation of gram-negative bacteria and/or the products of bacterial

growth. But it can ALSO be from common other infections. Things like

dental infections (gingivitis, peridontis) or GI disease like GERD can

injure the body enough to result in the placing of large amounts of

endotoxins into the bloodstream.

Amounts of mycotoxin that would otherwise not have clinically

measurable levels, then become toxic to living cells and cause cell

death. This may explain why yet another subset of people seem to be

more susceptible to injury from mold.

These exposures seem to me to BE ADDITIVE... So, people also exposed

to bacteria, such as raw sewage or coliform bacteria, or the dust from

them, or animal feces from vermin, or a person with GERD, or celiac

disease, or bad teeth, might be expected to get sicker quicker, as Dr.

Shoemaker might say.. They would get sick OR SENSITIZED MUCH MORE

RAPIDLY when ADDITIONALLY exposed to trichothecene mycotoxins

(verified), (and most probably also)other mycotoxins, MVOCs..in a

water damaged building,

Toxicol Sci. 2006 Aug;92(2):445-55. Epub 2006 May 9.

http://toxsci.oxfordjournals.org/cgi/reprint/92/2/445 (full text available)

Toll-like receptor priming sensitizes macrophages to

proinflammatory cytokine gene induction by deoxynivalenol and other

toxicants.

Pestka J, Zhou HR.

Department of Food Science and Human Nutrition, and Center for

Integrative Toxicology, Michigan State University, East Lansing,

48824, USA. pestka@...

Activation of the innate immune system might predispose a host to

toxicant-induced inflammation. In vitro macrophage models were

employed to investigate the effects of preexposure to Toll-like

receptor (TLR) agonists on induction of proinflammatory cytokine gene

expression by the trichothecene mycotoxin deoxynivalenol (DON) and

other toxicants. Priming of the murine RAW 264.7 macrophage line or

peritoneal murine macrophages with the TLR4 agonist lipopolysaccharide

(LPS) at 100 ng/ml for 4, 8, and 16 h significantly increased

DON-induced IL-1beta, IL-6, and TNF-alpha mRNA expression as compared

to LPS or DON alone. The minimum LPS concentration for sensitization

of both cell types was 1 ng/ml. LPS priming also potentiated IL-1beta

mRNA induction by DON in human whole-blood cultures, suggesting the

relevance of the murine findings. As observed for LPS, preexposure to

TLR agonists including zymosan (TLR2), poly (I:C) (TLR3), flagellin

(TLR5), R848 (TLR7/8), and ODN1826 (TLR9) sensitized RAW 267.4 cells

to DON-induced proinflammatory gene expression. Amplified

proinflammatory mRNA expression was similarly demonstrated in

LPS-sensitized RAW 264.7 cells exposed to the microbial toxins

satratoxin G, Shiga toxin, and zearalenone as well as the

anthropogenic toxicants nickel chloride, triphenyltin,

2,4-dinitrochlorobenzene, and 2,3,7,8-tetrachlorodibenzodioxin. The

results suggest that prior TLR activation might render macrophages

highly sensitive to subsequent induction of proinflammatory gene

expression by xenobiotics with diverse mechanisms of action.

Publication Types:

* Research Support, N.I.H., Extramural

PMID: 16687389 [PubMed - indexed for MEDLINE]

Toxicol Appl Pharmacol. 2006 Feb 15;211(1):53-63. Epub 2005 Jul 11.

LPS priming potentiates and prolongs proinflammatory cytokine

response to the trichothecene deoxynivalenol in the mouse.

Islam Z, Pestka JJ.

Department of Microbiology and Molecular Genetics, Michigan State

University, East Lansing, MI 48824, USA.

Simultaneous exposure to lipopolysaccharide (LPS) markedly

amplifies induction of proinflammatory cytokine expression as well as

IL-1-driven lymphocyte apoptosis by trichothecene deoxynivalenol (DON)

in the mouse. The purpose of this research was to test the hypothesis

that LPS priming will sensitize a host to DON-induced proinflammatory

cytokine induction and apoptosis. In mice primed with LPS (1 mg/kg bw)

ip. and treated 8 h later with DON po., the minimum DON doses for

inducing IL-1alpha, IL-1beta, IL-6 and TNF-alpha serum proteins and

splenic mRNAs were significantly lower than the DON doses required for

vehicle-primed mice. LPS priming also decreased onset time and

dramatically increased magnitude and duration of cytokine responses.

LPS-primed mice maintained heightened sensitivity to DON for up to 24

h. LPS priming doses as low as 50 microg/kg bw evoked sensitization.

DNA fragmentation analysis and flow cytometry also revealed that mice

primed with LPS (1 mg/kg) for 8 h and exposed to DON (12.5 mg/kg)

exhibited massive thymocyte loss by apoptosis 12 h later compared to

mice exposed to DON or LPS alone. LPS priming decreased DON-induced

p38 and ERK 1/2 phosphorylation suggesting that enhanced

mitogen-activated protein kinase activation was not involved in

increased cytokine responses. Taken together, exposure to LPS rendered

mice highly susceptible to DON induction of cytokine expression and

this correlated with increased apoptosis in the thymus.

Publication Types:

* Comparative Study

* Research Support, N.I.H., Extramural

PMID: 16009389 [PubMed - indexed for MEDLINE]

On Sun, Sep 14, 2008 at 11:08 AM, mlmj75 <MLMJ75@...> wrote:

>

>

>>

>> I've noticed that there is quite a bit of science on endotoxin

> exposure, and

>> that endotoxin levels are quite high in water damaged buildings,

>> particularly ones that involve flooding or similar.

>>

>> Why doesn't this get brought up more? Its obvious to me that it

> matters

>> substantially.

>>

>> Clean dry buildings don't have these high endotoxin levels, water

> damaged

>> buildings do.

>

> I totally agree with you. When one gets sick in a damp building,

> there is ususlly a unique " cocktail " of exposure which includes

> fungi, bacteria and yeasts. As far as I am concerned, it is the mix

> that makes you sick.

>

>

>

>