#1 ACOEM EXPOSED, A CASE STUDY IN SHAM PEER REVIEW & CONFLICTS OF INTEREST

[Guest guest]

Doug,

I am really glad you have opened this line of discussion on .

It's time that people understand what they are really up against. I may have

to do this in parts, but this is the paper that got the attention of the Wall

Street Journal writer, Armstrong. It goes into detail about exactly

what ACOEM did to legitimize Garbage science that has devastated the lives of

so many on this board by misinforming the physicians of America. And then the

US Chamber Commerce promoted the misinformation to financial stakeholders

such as the insurance, building, real estate and mortgage industries.

I have not copyrighted this paper. Anyone is welcome to use any information

they wish from it in any way the desire. We have sent this paper to the

Federal GAO, along with MANY others, to assist with their audit of the mold

issue. We have shared this paper with several Federal legislators. If anyone

wants a copy of it in it's entirety. (24 pages) Send me an email.

Sharon Kramer

ACOEM Exposed.

Mrs. Sharon N. Kramer, BBA, Business and Marketing

A Case Study of Sham Peer Review & Conflicts of Interest in Modern Medicine

- The Rats That Are Saving the Insurance Industry Billions -

ACOEM Exposed

Page 1

The American College of Occupational and Environmental Medicine (“ACOEMâ€)

has at best let itself be used, and at worst it has committed intellectual

fraud over the mold issue. While its members flourished, the lives of many have

been damaged. On October 27, 2002 the ACOEM endorsed an “Evidence-based

Statement†inferring that illnesses caused by indoor mold are not possible.

The

paper became and remains the

organization’s official position on the subject of illnesses caused by

indoor molds and mycotoxins. ACOEM did not reveal that this paper was

commissioned

by ACOEM in an apparent effort to defend or prevent lawsuits caused by mold,

nor that it was prepared by hand picked consultants sought out and recruited

by ACOEM, persons who were knownwitnesses for the insurance industry or

decidedly sympathetic to the viewpoint wanted.

The conclusions espoused by the Statement ignored the state of published

science and all of its own 83 references; was not properly peer reviewed; and

supports its “conclusions†without logical reference to any accepted

standard

of science or legitimate scientific research studies. Stripped of its jargon a

good high school biology student would see through it.

Nonetheless ACOEM endorsed it on October 27, 2002. In early 2003 the

Manhattan Institute paid the authors $40,000 to remake the statement into plain

English for the business stakeholder community. The layman’s translation –

“Thus

the notion that toxic mold is an insidious secret killer as so many media

reports and trial lawyers would claim is ‘Junk Science’ unsupported by

actual

scientific study.†But by July 2003, a peer reviewed paper published by the

American Society for Microbiology said “Mycotoxins are secondary metabolites

produced by microfungi that are capable of causing disease and death in humans

and other animals.â€1 The science continues to accumulate up to and including

a paper published March 2006 in

Environmental Health Perspectives that suggests that neurotoxicity and

inflammation within the nose and brain are potential adverse health effects of

exposure to satratoxins and Stachybotrys in the indoor air of water-damaged

buildings.2

1 Clin Microbiol Rev. 2003 July; 16(3): 497–516. doi:

10.1128/CMR.16.3.497-516.2003.

Copyright © 2003, American Society for Microbiology “Mycotoxins†by J. W.

1* and M. Klich2

2 Environmental Health Perspectives (The National Institute of Environmental

Health Sciences,

National Institutes of Health, U.S. Department of Health and Human Services)

“Satratoxin G from the

Black Mold Stachybotrys chartarum Evokes Olfactory Sensory Neuron Loss and

Inflammation in the

Murine Nose and Brainâ€, Zahidul Islam, Jack R. Harkema, and J. Pestka

doi:10.1289/ehp.8854

(available online Feb. 27, 2006 at _http://dx.doi.org/_ (http://dx.doi.org/) )

ACOEM Exposed.

Page 2

Many of ACOEM’s members derive the bulk of their income directly or

indirectly from the insurance industry, as they evaluate and treat injured

workers on

behalf of insurers and employers. These medical professionals owe a duty to

their patients which outweighs any commercial obligations to their

paymasters. Some of ACOEM’s members have enjoyed very substantial incomes

arising from

litigious use of the 2002 paper to deny liability, indeed to deny illness.

Conversely many sick Americans have not received medical treatment because of

it, since their insurance carriers deny coverage citing the ACOEM paper. The

carriers then hire the paper’s authors, along with their associates and

fellow

travelers, as the industry’s ‘expert’ witnesses to defend the deceit in

the

courts. Other patients lose out because their physicians are misinformed by

the ACOEM paper.

Under the guise of a ‘review’ piece, this ACOEM cornerstone of 2002

determines that it is not plausible that humans may become sick from exposure to

airborne indoor mycotoxins. None of the 83 documents named as references came to

this conclusion. None of the current research in the mold field in 2002, the

field purportedly being reviewed’, came to the same conclusion. This ‘

determination’ was based solely on the

authors’ own faulty logic and math calculations regarding the results of one

study of rats3 published two years earlier. No research before or since has

come to this conclusion, other than a rehashed repeat paper for the Manhattan

Institute, another industry grouping, written a few months later by the same

ACOEM authors for a $40,000 fee.

It is obvious that controlled experimental studies capable of directly

substantiating human mold illness cannot be performed. This is due to the legal,

moral and practical difficulties of asking humans to volunteer for a

prospective trial involving inhalation of varying amounts of potentially life

altering

toxins which have been shown (in vivo and in vitro) to be very dangerous.

[but then we know that a gunshot wound to the head is dangerous and we don’t

do

scientific studies of causation for that either.] Notwithstanding this

practical difficulty, the CDC as at 1.31.2006 offers the following on its web

site:

“Clinical description

'Trichothecene mycotoxins might be weaponized and dispersed through the air

or mixed in food or beverages. Initially, route-specific effects are

typically prominent. Dermal exposure leads to burning pain, redness, and

blisters,

and oral exposure leads to vomiting and diarrhea. Ocular exposure might result

in blurred vision, and inhalational exposure might cause nasal irritation and

cough. Systemic symptoms can develop with all routes of exposure and might

include weakness, ataxia, hypotension, coagulopathy, and

death (1).†4

3 Reduction of Pulmonary Toxicity of Stachybotrys chartarum Spores by

Methanol Extraction of

Mycotoxins, Rao, Brain and Burge. June 2000 in Applied & Environmental

Microbiology.

4 _www.cdc.gov_ (http://www.cdc.gov) and Search for Trichothecenes. Paper

Attached. Exhibit “Aâ€

ACOEM Exposed.

Page 3

These are the identical symptoms that have been observed in many who are

exposed to mycotoxins within a damp indoor environment. An EPA Science and

Ethics study has found that “uncertainties associated with animal data are

reflected by the routine use of a 10-fold interspecies uncertainty factor when

extrapolating from laboratory animals to humans.†Yet, based on self-serving

and

deeply flawed calculations applied to faulty data extrapolated from one poorly

designed study of rats, following a cynically prejudiced and

pre-ordained ‘peer review’ the ACOEM concluded in late 2002 that it is not

plausible for indoor mold to cause serious illness. And that is still ACOEM’s

position. Still! As to the actual state of scientific knowledge - the

leading rodent (mice) study was published in 2005 and it found that 3

Penicillium

toxins “common on damp materials in residential housingâ€â€¦ “provoke

compound

specific toxic responses …†and “Moreover that these toxins can stimulate

significant inflammatory responses in vivo might help explain some of the

indoor effects associated with Penicillium spore exposures in indoor

environments.â€

5 The methodology of this Canadian study provided a great deal of

scientific detail unlike the early, and thus crude, Rao rat study which was

misused by

the ACOEM authors. Notwithstanding an incomplete knowledge of mold, mold

particulates and mycotoxins in 1999 when the Rao rat study was performed,

nonetheless its authors concluded by

stating: “It has been hypothesized that the presence of S. chartarum in

occupied spaces is responsible for building-related adverse health effects,

including pulmonary hemorrhaging. Mycotoxins in the spores are the presumed

causative factor. Documenting such effects requires demonstrating that (i) S.

chartarum spores in the environment contained toxins; (ii) the observed effect

is

related to the toxin content rather than to

other spore components or other nonfungal factors; and (iii) sufficient

toxin exposure occurs to achieve a toxic dose. We provide evidence that there

is

a dose-related association between an acute exposure to toxin-containing S.

chartarum spores and measurable pulmonary responses. The consequences of

low-level chronic exposure remain to be investigated, as does the relevance of

the

rodent data to human exposure.â€

(Emphasis added)

The ACOEM statement when stripped of its verbosity says that the authors,

based on their misreading or misunderstanding of the flawed Rao rat study,

exacerbated by their incorrect assumptions, wrong math and faulty logic,

concluded that “spore concentrations†needed to cause illness “are

improbable and

inconsistent with reported spore concentrations†(Emphasis added). This is

just

plain wrong, it was wrong when written and is even more widely accepted as

wrong now. The truths of this matter are broad-ranging but they include the

fact that spores are far and away the least numerous of the poisoned

particulates that cause illness

– viz. “The … results using the aerosolisation chamber show that a

significantly higher 5 number of microbial propagules with diameters smaller

than

those of the spores is released from microbiologically contaminated surfaces

[59, 60].

“Inflammatory and Cytotoxic Responses in Mouse Lungs Exposed to Purified

Toxins from Building Isolated Penicillium brevicompactum Dierckx and P.

chrysogenum Thom.†In Toxicological Sciences 87(1), 213-222 (2005) Drs. Rand,

Giles,

Flemming, , Puniani.

ACOEM Exposed.

Page 4

Even with the sensitivity of the device used for the control of fragment

concentration (e.g., an optical

particle counter, such as Grimm OPC allowing descent to the level of 0.3 μm

for the particle diameter), the number of aerosolized fragments can be

several hundred times higher than the number of released intact spores from the

same surface area. The presence of the submicrometer propagules released in

such

a way can be documented by scanning electron microscope (SEM) analysis.†6

(Emphasis added) Although the Rao rat study, in hindsight and with the benefit

of after-acquired knowledge, was fundamentally flawed, even so the method

used by the ACOEM consultants in their 2002 paper to ‘determine’ that

mycotoxins in an indoor setting cannot plausibly cause human illness does not

meet

any of the elementary standards of fact or logic. It is a gross

mischaracterization of the Rao study to say that it provides scientific support

for the

ACOEM statement. For instance, using their bundle of wrong assumptions, wrong

math and faulty logic ACOEM says “Levels of exposure in the indoor

environment,

dose-response data in animals, and dose-rate considerations suggest that

delivery by the inhalation route of a toxic dose of mycotoxins in the indoor

environment is highly unlikely at best, even for the hypothetically most

vulnerable subpopulations.â€

This too is just plain wrong, it was wrong when written and is even more

widely accepted as wrong now. The truth appears to be that “Biological

aerosols

can penetrate into the human body through the nose, mouth and conjunctiva

epithelium, bronchi and alveoli, as well as the epidermis (mainly on hands)

[37]. In the human respiratory tract, the penetration depth and behaviour of

bioaerosol particles depends on their size, shape,

density, chemical composition and reactivity. Particles, which enter the

respiratory system can be deposited by 5 major mechanisms: impaction,

sedimentation, diffusion, interception and electrostatic precipitation [10, 16,

109,

142]. The majority of particles with a diameter greater than 10 μm, and up to

80% of particles with diameters between 5- 10 μm, is trapped in the

nasopharyngeal region due to inertial impaction and centrifugal condensation

resulting

from anatomic formation of these stages of the respiratory tract

(where the air stream gain has the highest velocity) [128, 171]. For

particles with an elevated ratio between their length and diameter (e.g, for

fungal

spore chains), these 2 processes are assisted by the interception mechanism

[142]. For particles with diameters above 0.5 μm, the primary deposition

mechanisms are sedimentation and impaction, which take place in bronchi,

bronchioles, and alveoli, where the air velocity is low [118] and a probability

of

deposition is directly proportional to the residence time [171]. For particles

of less than 0.5 μm, diffusion is the major mechanism for particle separation

from the air stream. This process depends (inversely proportional) on

particle diameter and is supported by electrostatic precipitation resulting

from

interaction between surface and particle charges penetrate deeper in to the

lungs and are deposited almost solely through the diffusion mechanism.†7

[114,

115, 171].

Submicron particles, especially these below 0.1μm, 6 Exhibit “Bâ€

FILAMENTOUS MICROORGANISMS AND THEIR FRAGMENTS IN INDOOR AIR

Department of Biohazards, Institute of Occupational Medicine and

Environmental Health, Sosnowiec,

Poland

ACOEM Exposed.

Page 5

ACOEM’s self-described “evidence-based statement†contains a number of

critical misstatements and concludes with “Current scientific evidence does

not

support the proposition that human health has been adversely affected by

inhaled mycotoxins in home, school, or office environments.†(Emphasis added)

Although carefully stated in the negative, viz “does not support†and

qualified

by “current scientific evidence†- this statement and much of the rest of

the paper is flawed. 8 Indeed the level of credulousness exhibited by ACOEM can

be judged by the 83 references cited by its authors – none of which supports

the “evidence-based†statement adopted by ACOEM that “Levels of exposure

in

the indoor environment, dose-response data in animals, and dose-rate

considerations suggest that delivery by the inhalation route of a toxic dose of

mycotoxins in the indoor environment is highly unlikely at best, even for the

hypothetically most vulnerable subpopulations.†Not one of the 83 cited

papers

concluded it is not plausible that people could inhale enough mycotoxins

within an indoor environment to cause illness. The only aspect of this

purported

review piece which supported the authors’ contention are the self-serving and

fallacious math calculations done by the authors themselves (cf. paragraphs

3, 8 & 9 of Dr. Lipsey’s enclosed affidavit ). Exhibit “D†9 is a

critique of

the ACOEM paper written by Ritchie Shoemaker MD, a physician who has

diagnosed and treated some 3,000 mold patients. These patients were not rats,

not

mice, not rabbits, they were people. Dr. Shoemaker has published peer reviewed

articles that contradict the entire thrust of ACOEM’s self –described “

evidence based statementâ€. Recently a group of leading mold physicians and

toxicologists refer to his work as having “met the highest levels of evidence

as

defined by the Agency for Healthcare Research and Quality necessary to provide

convincing evidence (AHRQ 2005)â€. (Emphasis added.)

Exhibit “E†is an affidavit provided recently by Dr. Lipsey, a

noted toxicologist with a Ph.D. in mold poisons and toxicology, qualified to

testify in state and federal courts having undergone numerous Frye and Daubert

hearings. He has 36 years of experience as a professor of toxicology, teacher,

industry spokesman and expert witness. He handles plaintiff and defense cases

equally and is a scientific article peer reviewer for

the Society of Toxicology, the American College of Toxicology and the

American Cancer Society.

In January 2006 Dr. Lipsey provided an affidavit 10 in which he stated in

relation to the ACOEM statement that: “2. …I have reviewed the study by

Rao,

Brain and Burge as published … upon which the Hardin and Kelman model 11 was

based.

7 Op. cit. – Ref. Ex. “Bâ€

8 Exhibit “C†History viz 1959, 1976, 1976, 1983, 1984, 1984, 1985, 1987,

1988, 1989, 1991,1991, 1992,

1993, 1993, 1994, 1998, 1999, 2001.

9 R. Shoemaker MD – Letter Exhibit “Dâ€

10 Exhibit “Eâ€

11 Two of the ACOEM authors.

Needless to say, I had some assistance with the science aspect of this

paper. The science is not my field of expertise, but the conflicts of interest

are. However, it does not require a scientist to understand that the authors of

the ACOEM mold statement erroneously applied some math to high dose rodent

study and FALSELY concluded the toxins from mold are " not plausible " to cause

human illness. That methodology is not now, nor has it ever been accepted

scientific methodology to form the conclusions it did.

Will post more of the 24 page paper tomorrow.

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