WHO: In experimental animals, trichothecenes are 40 times more toxic when inhaled than when given orally - why wasn't that included in ACOEM paper?

[Guest guest]

I thought this deserved a thread of its own..

Sharon C. Thank you - The reference is reference 98

http://whqlibdoc.who.int/bulletin/1999/Vol77-No9/bulletin_1999_77(9)_754-766.pdf

<http://whqlibdoc.who.int/bulletin/1999/Vol77-No9/bulletin_1999_77%289%29_754-76\

6.pdf>

" Trichothecenes

Trichothecenes are mycotoxins produced mostly by

members of the Fusarium genus, although other

genera (e.g. Trichoderma, Trichothecium, Myrothecium and

Stachybotrys) are also known to produce these

compounds. To date, 148 trichothecenes have been

isolated, but only a few have been found to

contaminate food and feed. The most frequent

contaminants are deoxynivalenol (DON), also

known as vomitoxin, nivalenol (NIV), diacetoxyscirpenol

(DAS), while T-2 toxin is rarer (12).

Common manifestations of trichothecene toxicity

are depression of immune responses and nausea,

sometimes vomiting (Table 5). The first recognized

trichothecene mycotoxicosis was alimentary toxic

aleukia in the USSR in 1932; the mortality rate was

60% (91). In regions where the disease occurred, 5±

40% of grain samples cultured showed the presence of

Fusarium sporotrichoides, while in those regions where the

disease was absent this fungus was found in only 2±8%

of samples. The severity of mycotoxicosis was related

to the duration of consumption of toxic grain. Such

severe trichothecene mycotoxicoses, the consequence

of continuous ingestion of toxins, have not been

recorded since this outbreak.

In several cases, trichothecene mycotoxicosis

was caused by a single ingestion of bread containing

toxic flour (95) or rice (92, 97).

*In experimental animals, trichothecenes are 40

times more toxic when inhaled than when given orally*

(98). Trichothecenes were found in air samples

collected during the drying and milling process on

farms (99), in the ventilation systems of private houses

(100) and office buildings (98), and on the walls of

houses with high humidity (100, 101) (Table 6). There

are some reports showing trichothecene involvement

in the development of ``sick building syndrome'' (98,

100). The symptoms of airborne toxicosis disappeared

when the buildings and ventilation systems were

*thoroughly cleaned* (100).

There are some reports that indicate that

trichothecenes may have been used as chemical

warfare agents in South-East Asia (Lao People's

Democratic Republic and Cambodia) (102, 103). "

The WHO paper footnote 98 refers to this paper:

Wanda Smoragiewicz, Bruno Cossette, Armel Boutard and Krzysztof Krzystyniak

Trichothecene mycotoxins in the dust of ventilation systems in office

buildings.

International archives of occupational and environmental health, 1993, 65:

113-117

Analysis of trichothecene mycotoxins in dust samples from ventilation

systems of office buildings was applied as a rapid and inexpensive method

for the detection of mycotoxins. Dust samples from three different office

spaces of the Montreal urban area, reportedly affected by the ldquosick

buildings syndromerdquo, were analysed by thin-layer chromatography (TLC).

Positive colour reaction on TLC plates with 4-(p-nitrobenzyl) pyridine,

specific for the 12,13-epoxy group in the trichothecene nucleus, was

obtained for the extracts of 0.5- to 50-g dust samples. The dust samples

contained at least four trichothecenes: T-2 toxin, diacetoxyscirpenol,

roridine A and T-2 tetraol. The results were confirmed by high-performance

liquid chromatography analysis. Screening of dust samples from air

ventilation systems of reportedly affected buildings provided direct

evidence of trichothecene mycotoxins, with the detection limit estimated as

0.4-4 ng/mg dust. Thus, the dust sample analysis is suggested as a rapid

technique for detecting the presence of mycotoxins in the dust of

ventilation systems.

Key words Trichothecene mycotoxins - Sick building syndrome - Airborne

toxicosis - Indoor air pollution - Microbial contaminants

In my opinion, the fact that the ACOEM *COMPLETELY LEFT THIS FACT OUT* of

their oh-so-short overview of mycotoxin toxicity (which seemed to be based

on ingestional toxicity, NOT INHALED) Is a CARDINAL SIN OF OMISSION THAT

INVALIDATES THE ENTIRE WORK.

Another HUGE sin of omission, their leaving out the large body of work on

lipopolysaccaride endotoxin 'priming' of the toxicity of trichothecenes -

which ALSO POTENTIATES THEIR TOXICITY GREATLY.

They also left out the MCS-causing effects of MVOCs.

I think these omissions were intentional BECAUSE THESE ARE THE POINTS WHERE

THEIR ARGUMENT NO LONGER CAN BE ARGUED..