Re: effect of mold on breast cancer patient

January 20, 2008

I'm sure you'll get much better answers from others, but I can give you an EASY

answer -

Mold and mycotoxins are KNOWN to be hazardous to those who are

immunocompromised, and a cancer survivor would nearly certainly meet that test.

(The rest of us are still fighting to prove that they cause immunosuppression as

well, but that's another story).

If you do a search on 'mold' and 'immunocompromised' you should be able to

come up with enough information to take it to Legal Aid and have someone write a

letter to your human resources saying it could jeopardize her health. Better

yet, do the search in PubMed - there should be plenty of medical journal

articles on this subject. This should be something that would get her

'protection' (such as it is under this Administration which has been working to

dismantle these protections) under the Americans with Disabilities Act.

Best of luck - keep us posted.

~Haley

toxsickniagara <toxsickniagara@...> wrote:

One of my coworkers was recently diagnosed with breast cancer. Her

office is being reassigned to the basement of our building.

Stachybotrys and Aspergillus were removed in 2004 and 2005, and we are

not quite sure that all the mold was removed. We continue to have

problems with plumbing leaks, water intrusion, groundwater flooding,

sewer backups, and uncontrolled humidity. She is concerned that after

her breast surgery and during her radiation treatments that the

conditions in her office area may harm her health. Does anyone have a

link to any papers written on the effect of toxic mold on breast

cancer patients?

January 20, 2008

May in his book " My house is killing me " that one should not

live or work in a basement for health reasons, in Chapter 9 on Finished

Basements.

>

> One of my coworkers was recently diagnosed with breast cancer. Her

> office is being reassigned to the basement of our building.

> Stachybotrys and Aspergillus were removed in 2004 and 2005,

January 20, 2008

Thank you Barb - that reminded me that I have a book by May -

" My Office is Killing Me. " There is some info there about Aflotoxins

from Aspergillus mold, and about moisture and molds in basements. I

had forgotten about that. Thanks for the reminder.

>

> May in his book " My house is killing me " that one should not

> live or work in a basement for health reasons, in Chapter 9 on

Finished

> Basements.

>

January 21, 2008

Okay, you should contact the autors of these studies for more info. I

am just copying and pasting here..

But, as I read this, many studies have shown that certain environments

that contain lots of bacteria - like basements that have seen

FLOODING, have BACTTERIAL ENDOTOXINS that strongly potentiate mold

effects. Also mold emits MVOCs while it is growing, complex volatile

chemicals.. They do other things.. So these situations are more

accurately described as MOLD + BACTERIA + MVOC situations, not mold

alone. The situation you described sounds like one of them. They are

the most dangerous. Sounds like they are trying to send her a message

that she might be better off elsewhere??? Huh? She should contact a

lawyer.

Mold toxins are potentiated very strongly by bacterial endotoxins,

such as are found in places that are damp and have seen sewer

intrusion or dead animals, etc. (like moldy basements) That makes the

cytoxic and inflammatory effects of the mold many more times stronger.

Stachybotrys often does not show up on tests. See the last abstract

for why. Were all the wall cavities cleaned out? Does it still smell

damp? What is the relative humidity down there, does it go above 50%

ever? (like at night)

Also, spore tests are notoriously GOOD at NOT SHOWING STACHYBOTRYS. In

fact, they rarely show it even when its really bad.

Thats why spore tests should not be used in post remediation clearance.

Toxicol Sci. 2007 Aug;98(2):526-41. Epub 2007 May 4.Click here to read Links

Neurotoxicity and inflammation in the nasal airways of mice

exposed to the macrocyclic trichothecene mycotoxin roridin a: kinetics

and potentiation by bacterial lipopolysaccharide coexposure.

Islam Z, Amuzie CJ, Harkema JR, Pestka JJ.

Department of Food Science and Human Nutrition, Michigan State

University, East Lansing, Michigan 48824, USA.

Macrocyclic trichothecene mycotoxins produced by indoor air molds

potentially contribute to symptoms associated with damp building

illnesses. The purpose of this investigation was to determine (1) the

kinetics of nasal inflammation and neurotoxicity after a single

intranasal instillation of roridin A (RA), a representative

macrocyclic trichothecene; and (2) the capacity of lipopolysaccharide

(LPS) to modulate RA's effects. C57Bl/6 female mice were intranasally

instilled once with 50 mul of RA (500 mug/kg body weight [bw]) in

saline or saline only and then nose and brain tissues were collected

over 72 h and processed for histopathologic and messenger RNA (mRNA)

analysis. RA-induced apoptosis specifically in olfactory sensory

neurons (OSNs) after 24 h postinstillation (PI) causing marked atrophy

of olfactory epithelium (OE) that was maximal at 72 h PI.

Concurrently, there was marked bilateral atrophy of olfactory nerve

layer of the olfactory bulbs (OBs) of the brain. In the ethmoid

turbinates, upregulated messenger RNA (mRNA) expression of the

proapoptotic gene FAS and the proinflammatory cytokines tumor necrosis

factor-alpha, interleukin (IL)-6, IL-1, and macrophage inhibitory

protein-2 was observed from 6 to 24 h PI, whereas expression of

several other proapoptotic genes (PKR, p53, Bax, and caspase-activated

DNAse) was detectable only at 24 h PI. Simultaneous exposure to LPS

(500 ng/kg bw) and a lower dose of RA (250 mug/kg bw) magnified

RA-induced proinflammatory gene expression, apoptosis, and

inflammation in the nasal tract. Taken together, the results suggest

that RA markedly induced FAS and proinflammatory cytokine expression

prior to evoking OSN apoptosis and OE atrophy and that RA's effects

were augmented by LPS.

PMID: 17483119 [PubMed - indexed for MEDLINE]

Deoxynivalenol and satratoxin G potentiate proinflammatory cytokine

and macrophage inhibitory protein 2 induction by Listeria and

Salmonella in the macrophage.

Mbandi E, Pestka JJ.

Department of Food Science and Human Nutrition and Center for

Integrative Toxicology, Michigan State University, East Lansing,

Michigan 48824, USA.

Health risks from microbial pathogens and toxins encountered in food

and the environment continue to be of worldwide concern. The purpose

of this research was to test the hypothesis that trichothecene

mycotoxins amplify inflammatory responses to foodborne bacterial

pathogens. We assessed the capacity of deoxynivalenol (DON) and

satratoxin G (SG) to potentiate chemokine and proinflammatory cytokine

production in RAW 264.7 murine macrophages induced by Listeria

monocytogenes and Salmonella Typhimurium. When macrophage cultures

were incubated with killed irradiated suspensions of the pathogens for

24 h, the minimum Listeria concentrations for induction of macrophage

inhibitory protein 2 (MIP-2), interleukin-1beta (IL-beta), IL-6, and

tumor necrosis factor alpha (TNF-alpha) were 0.01, 0.01, 1.0, and 1.0

microg/ml (P < 0.05) and the minimum Salmonella concentrations were

0.01, 0.01, 0.1, and 0.1 microg/ml, respectively (P < 0.05). Induction

of all four mediators by both pathogens was potentiated by DON (at 100

and 250 ng/ml); observed responses were significantly higher than

predicted additive responses (P < 0.05). SG (at 2 and 5 ng/ml) also

significantly amplified induction of IL-1beta and TNF-alpha (P < 0.05)

by both Listeria and Salmonella. These results indicate that DON

encountered in Fusarium-contaminated food and SG from

Stachybotrys-contaminated indoor environments could magnify innate

inflammatory responses to foodborne bacterial pathogens.

PMID: 16786854 [PubMed - indexed for MEDLINE]

Toxicol Sci. 2006 Aug;92(2):445-55. Epub 2006 May 9.Click here to read Links

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.

PMID: 16687389 [PubMed - indexed for MEDLINE]

Toxicol In Vitro. 2006 Sep;20(6):899-909. Epub 2006 Mar 6.Click here

to read Links

In vitro effects of trichothecenes on human dendritic cells.

Hymery N, Sibiril Y, Parent-Massin D.

Laboratoire de Toxicologie Alimentaire, EA 3880 UniversitÃ© de

Bretagne Occidentale, TechnopÃ´le Brest-Iroise 29280 PlouzanÃ©, France.

The aim of this work was to study the in vitro effects of

trichothecenes on human dendritic cells. Trichothecenes are mycotoxins

produced by fungi such as Fusarium, Myrothecium, and Stachybotrys. Two

aspects have been explored in this work: the cytotoxicity of

trichothecenes on immature dendritic cells to determine IC 50

(inhibition concentration), and the effects of trichothecenes on

dendritic cell maturation process. Two mycotoxins (T-2 and DON) known

to be immunotoxic have been tested on a model of monocyte-derived

dendritic cells culture. Cytotoxic effects of T-2 toxin and DON on

immature dendritic cells showed that DON is less potent than T-2

toxin. The exposure to trichothecenes during dendritic cell maturation

upon addition of LPS or TNF-alpha markedly inhibited the up-regulation

of maturation markers such as CD-86, HLA-DR and CCR7. Features of LPS

or TNF-alpha -mediated maturation of dendritic cells, such as IL-10

and IL-12 secretions and endocytosis, were also impaired in response

to trichothecenes treatment. These results suggest trichothecenes have

adverse effects on dendritic cells and dendritic cell maturation

process.

PMID: 16517116 [PubMed - indexed for MEDLINE]