Re: Ron Gots writes: Mycotoxins: Little evidence of harm from indoor air exposure

[Guest guest]

This guy is an IDIOT, a shill for the chemical industry and everyone in

the environmental movement knows of the fraud.

I guess his pathetic ego needed some stroking and he had to shoot his

mouth off again!

Angel

On Wed, 22 Oct 2003, Barbara Herskovitz wrote:

> Date: Wed, 22 Oct 2003 18:48:44 -0400

> From: Barbara Herskovitz <bherk@...>

> Reply-

> Sick Buildings Information & Support < >

> Subject: [] Ron Gots writes: " Mycotoxins: Little evidence

> of harm from indoor air exposure "

>

> http://www.industrialsourcebook.com/cgi-bin/archivef.pl?id=576

>

> Research Report - Mycotoxins: Little evidence of harm from indoor air exposure

>

> September 2003

>

> Author: E. Gots, M.D., Ph.D.

>

> In the following report, E. Gots, M.D., Ph.D., principal with the

International Centre for Toxicology and Medicine (ICTM) summarizes the latest

research on airborne toxins and why broad conclusions about the harmful effects

in our indoor environment are poorly supported.

>

> The media and public continue to be concerned about health risks resulting

from exposure to mycotoxins produced by stachybotrys and other fungi present in

indoor air. Mycotoxins are by-products of the natural life-cycle of all fungi.

Their production is dependent on complex interactions among numerous factors,

including nutrition availability, moisture, temperature, and competition from

other microorganisms.

>

> The characteristics, type, and quantity of mycotoxins produced by any species

of fungi vary widely. The mere presence of a toxigenic mould detected in indoor

air does not mean that mycotoxins are also present. Of particular importance is

the quantity that might be present. Several investigators have attempted to shed

some light on this issue.

>

> A review of the literature indicates that acute and long-term chronic effects

are more commonly associated with extremely high inhalation concentrations. The

term " organic dust toxic syndrome " (ODTS) has been used in referring to

respiratory problems such as pulmonary mycotoxicosis, grain fever, farmer's

lung, mill fever, and inhalation fever. Exposures documented for ODTS are

described as extremely thick airborne dust or fog. Total microbial

concentrations related to these diseases are reported, ranging from one hundred

thousand to one billion spores per cubic meter. Such concentrations are rarely,

if ever, observed in the indoor ambient air of residential or commercial

buildings.

>

> The majority of animal in vivo data on toxicity of mycotoxins are limited to

studies of mice, rats and guinea pigs, in which lethal concentrations are

identified. In these studies, the doses are administered to a test animal in

ways that are not equivalent to human inhalation exposures. Also, there is

variability in animal sensitivity, with rats being most sensitive. Even testing

the more sensitive rat with a fusarium trichothecene (T-2), no mortality

occurred at a single administration of 1.0 mg/m3. Data about the quantity of T-2

recovered in a single spore are not available. However, it has been reported

that per spore concentrations of satratoxin H in stachybotrys spores is

estimated at 0.0004 ng/spore. Using this value, Hardin, Saxin and Kelman, in a

recent, excellent review, have estimated that 10 billion spores would be

required to reach 1.0 mg of this toxin in a cubic meter of air.

>

> Similar requirements for high spore counts in ambient air have been reported

by others investigating the potential for airborne mycotoxins from other fungal

species. Fischer et al. estimated that to obtain 1 ng of an Aspergillus

mycotoxin would require an airborne density of 107 cfu/m3.

>

> To place these estimates in a more human context it is useful to review

Burge's risk model. In this model, the potential accumulation of mould toxin in

the lung could be estimated based on indoor ambient air spore counts. Making

assumptions about spore content and human inhalation frequency and duration,

results of this model suggest that it would require 1,100 days of an individual

inhaling 100 spores/m3 to accumulate 1 ng of a toxin in the lung.

>

> In animal dose-response data associating pulmonary inflammation and hemorrhage

with exposure to stachybotrus chartarum, a no-effect dose of three million

spores/kg body weight has been identified.

>

> Airborne concentrations representing human doses comparable to this no-effect

dose have been estimated recently by Hardin et al. Their calculations were based

on an assumption that all of the airborne spores would be retained in the human

lung and on the application of standard risk assessment default values. Thus,

the animal no-effect dose is comparable " to a continuous 24-hour exposure to 2.1

x 106 spores/m3 for infants, 6.6 x 106 spores/m3 for school-aged children, and

15.3 x 106 spores/m3 for an adult. "

>

> Hardin et al. emphasize that these no-effect estimates represent an

over-estimate of risk because they have assumed that the toxic effect would be

the same despite a major difference in route of exposure between animals and

humans. Cumulative doses experienced over time-periods more typical of human

exposures would be less acutely toxic than the large single doses administered

to test animals. These larger doses could overwhelm inherent, internal

protective measures. When Hardin et al. made the assumption that the animal

no-effect dose represented a one minute administration, the estimates for a

human comparable dose become 3.0 x 109 spores/m3 for infants, 9.5 x 109

spores/m3 for school-aged children, and 22.0 x 109 spores/m3 for adults.

>

> Finally, using data from a repeat-dose study in which a concentration of 2.8 x

105 stachybotrys spores/kg produced severe pulmonary inflammation, but no

hemorrhaging, Hardin et al. estimated human equivalent doses. Applying the same

assumptions, the estimated airborne concentration required to " deliver the

non-hemorrhagic cumulative three-week dose of 2.8 x 105 stachybotrys spores/kg "

is 9400 spores/m3 for infants, 29,000 spores/m3 or school-aged children, and

68,000 spores/m3 for adults. I agree with the authors' assessment that these

levels are improbable for residential and commercial indoor ambient air and

inconsistent with reported airborne concentrations.

>

> Cause and effect

> Several problems need to be resolved before we can begin gathering evidence of

an association between inhalation exposure to mycotoxins and adverse health

outcomes. One problem is the fact that there is insufficient evidence with which

one can evaluate the relevance of mycotoxins produced in a laboratory culture

setting as predictors of those that might be present in indoor ambient air.

>

> Data supporting comparability are extremely limited. A recent study has

revealed that when comparing strains of mycotoxins present in pure cultures and

extracted from spores, there is only a 60 percent match. Some fungal species

have more consistent mycotoxin production than others. For example, aspergillus

fumagatus, penicillium polonicum and penicillium crustosum exhibit consistent

results between pure culture and spore extracts. Aspergillus niger and

paecilomyces variotii reveal inconsistent results.

>

> There is currently no research on differences that might exist with

stachybotrys species, today's popular mould concern. However, these data make it

clear that one cannot assume that mycotoxins detected in laboratory cultures

would be the same as those potentially present in spores or on particulates in

ambient air, simply because a particular mould has been detected. We currently

have no reliable analytical methods with which ambient air samples can be

evaluated for the presence of mycotoxins.

>

> By E. Gots, M.D., Ph.D., Principal, International Center for Toxicology

and Medicine (ICTM) regots@...

>

" If having endured much, we at last asserted our 'right to know' and if,

knowing, we have concluded that we are being asked to take senseless and

frightening risks, then we should no longer accept the counsel of those

who tell us that we must fill our world with poisonous chemicals, we

should look around and see what other course is open to us. "

Carson

" My toxicasa (world) is your toxicasa (world). "

Judith Goode

[Guest guest]

I agree, a shill.

----- Original Message -----

From: Angel MCS

Sick Buildings Information & Support

Sent: Wednesday, October 22, 2003 11:32 PM

Subject: Re: [] Ron Gots writes: "Mycotoxins: Little evidence of harm from indoor air exposure"

This guy is an IDIOT, a shill for the chemical industry and everyone inthe environmental movement knows of the fraud.I guess his pathetic ego needed some stroking and he had to shoot hismouth off again!AngelOn Wed, 22 Oct 2003, Barbara Herskovitz wrote:> Date: Wed, 22 Oct 2003 18:48:44 -0400> From: Barbara Herskovitz <bherk@...>> Reply- > Sick Buildings Information & Support < >> Subject: [] Ron Gots writes: "Mycotoxins: Little evidence> of harm from indoor air exposure">> http://www.industrialsourcebook.com/cgi-bin/archivef.pl?id=576>> Research Report - Mycotoxins: Little evidence of harm from indoor air exposure>> September 2003>> Author: E. Gots, M.D., Ph.D.>> In the following report, E. Gots, M.D., Ph.D., principal with the International Centre for Toxicology and Medicine (ICTM) summarizes the latest research on airborne toxins and why broad conclusions about the harmful effects in our indoor environment are poorly supported.>> The media and public continue to be concerned about health risks resulting from exposure to mycotoxins produced by stachybotrys and other fungi present in indoor air. Mycotoxins are by-products of the natural life-cycle of all fungi. Their production is dependent on complex interactions among numerous factors, including nutrition availability, moisture, temperature, and competition from other microorganisms.>> The characteristics, type, and quantity of mycotoxins produced by any species of fungi vary widely. The mere presence of a toxigenic mould detected in indoor air does not mean that mycotoxins are also present. Of particular importance is the quantity that might be present. Several investigators have attempted to shed some light on this issue.>> A review of the literature indicates that acute and long-term chronic effects are more commonly associated with extremely high inhalation concentrations. The term "organic dust toxic syndrome" (ODTS) has been used in referring to respiratory problems such as pulmonary mycotoxicosis, grain fever, farmer's lung, mill fever, and inhalation fever. Exposures documented for ODTS are described as extremely thick airborne dust or fog. Total microbial concentrations related to these diseases are reported, ranging from one hundred thousand to one billion spores per cubic meter. Such concentrations are rarely, if ever, observed in the indoor ambient air of residential or commercial buildings.>> The majority of animal in vivo data on toxicity of mycotoxins are limited to studies of mice, rats and guinea pigs, in which lethal concentrations are identified. In these studies, the doses are administered to a test animal in ways that are not equivalent to human inhalation exposures. Also, there is variability in animal sensitivity, with rats being most sensitive. Even testing the more sensitive rat with a fusarium trichothecene (T-2), no mortality occurred at a single administration of 1.0 mg/m3. Data about the quantity of T-2 recovered in a single spore are not available. However, it has been reported that per spore concentrations of satratoxin H in stachybotrys spores is estimated at 0.0004 ng/spore. Using this value, Hardin, Saxin and Kelman, in a recent, excellent review, have estimated that 10 billion spores would be required to reach 1.0 mg of this toxin in a cubic meter of air.>> Similar requirements for high spore counts in ambient air have been reported by others investigating the potential for airborne mycotoxins from other fungal species. Fischer et al. estimated that to obtain 1 ng of an Aspergillus mycotoxin would require an airborne density of 107 cfu/m3.>> To place these estimates in a more human context it is useful to review Burge's risk model. In this model, the potential accumulation of mould toxin in the lung could be estimated based on indoor ambient air spore counts. Making assumptions about spore content and human inhalation frequency and duration, results of this model suggest that it would require 1,100 days of an individual inhaling 100 spores/m3 to accumulate 1 ng of a toxin in the lung.>> In animal dose-response data associating pulmonary inflammation and hemorrhage with exposure to stachybotrus chartarum, a no-effect dose of three million spores/kg body weight has been identified.>> Airborne concentrations representing human doses comparable to this no-effect dose have been estimated recently by Hardin et al. Their calculations were based on an assumption that all of the airborne spores would be retained in the human lung and on the application of standard risk assessment default values. Thus, the animal no-effect dose is comparable "to a continuous 24-hour exposure to 2.1 x 106 spores/m3 for infants, 6.6 x 106 spores/m3 for school-aged children, and 15.3 x 106 spores/m3 for an adult.">> Hardin et al. emphasize that these no-effect estimates represent an over-estimate of risk because they have assumed that the toxic effect would be the same despite a major difference in route of exposure between animals and humans. Cumulative doses experienced over time-periods more typical of human exposures would be less acutely toxic than the large single doses administered to test animals. These larger doses could overwhelm inherent, internal protective measures. When Hardin et al. made the assumption that the animal no-effect dose represented a one minute administration, the estimates for a human comparable dose become 3.0 x 109 spores/m3 for infants, 9.5 x 109 spores/m3 for school-aged children, and 22.0 x 109 spores/m3 for adults.>> Finally, using data from a repeat-dose study in which a concentration of 2.8 x 105 stachybotrys spores/kg produced severe pulmonary inflammation, but no hemorrhaging, Hardin et al. estimated human equivalent doses. Applying the same assumptions, the estimated airborne concentration required to "deliver the non-hemorrhagic cumulative three-week dose of 2.8 x 105 stachybotrys spores/kg" is 9400 spores/m3 for infants, 29,000 spores/m3 or school-aged children, and 68,000 spores/m3 for adults. I agree with the authors' assessment that these levels are improbable for residential and commercial indoor ambient air and inconsistent with reported airborne concentrations.>> Cause and effect> Several problems need to be resolved before we can begin gathering evidence of an association between inhalation exposure to mycotoxins and adverse health outcomes. One problem is the fact that there is insufficient evidence with which one can evaluate the relevance of mycotoxins produced in a laboratory culture setting as predictors of those that might be present in indoor ambient air.>> Data supporting comparability are extremely limited. A recent study has revealed that when comparing strains of mycotoxins present in pure cultures and extracted from spores, there is only a 60 percent match. Some fungal species have more consistent mycotoxin production than others. For example, aspergillus fumagatus, penicillium polonicum and penicillium crustosum exhibit consistent results between pure culture and spore extracts. Aspergillus niger and paecilomyces variotii reveal inconsistent results.>> There is currently no research on differences that might exist with stachybotrys species, today's popular mould concern. However, these data make it clear that one cannot assume that mycotoxins detected in laboratory cultures would be the same as those potentially present in spores or on particulates in ambient air, simply because a particular mould has been detected. We currently have no reliable analytical methods with which ambient air samples can be evaluated for the presence of mycotoxins.>> By E. Gots, M.D., Ph.D., Principal, International Center for Toxicology and Medicine (ICTM) regots@...>"If having endured much, we at last asserted our 'right to know' and if,knowing, we have concluded that we are being asked to take senseless andfrightening risks, then we should no longer accept the counsel of thosewho tell us that we must fill our world with poisonous chemicals, weshould look around and see what other course is open to us." Carson"My toxicasa (world) is your toxicasa (world)." Judith GoodeFAIR USE NOTICE:This site contains copyrighted material the use of which has not always been specifically authorized by the copyright owner. We are making such material available in our efforts to advance understanding of environmental, political, human rights, economic, democracy, scientific, and social justice issues, etc. We believe this constitutes a 'fair use' of any such copyrighted material as provided for in section 107 of the US Copyright Law. In accordance with Title 17 U.S.C. 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