Origin of Junk Science over the Mold Issue

[Guest guest]

Below is a link to a paper I find fascinating. It details the history of

risk assessment. It helps to explain why random numbers such as LD50's based on

acute exposure linear modeling theories do not accurately portray human

exposures that are occurring within water damaged buildings.

This heavily promoted, industry friendly, type of modeling theory is the

bottleneck of why it has become common medical understanding that one cannot be

exposed to enough toxin producing microbial contaminants to experience

symptoms indicative of toxicity.

In a nutshell, it is misguided policy not founded in sound scientific

principles and ignores the implications of low dose, multiple exposures and all

epidemiological research/findings. This is the origin of the junk science

driving the medical misunderstanding over mold/mold toxin induced illnesses.

Risk assessment has morphed into financial risk management.

I pulled out some key phrases from the document.

Sharon

_http://www.environchttp://www.ehttp://www.envirhttp://wwwhtt_

(http://www.environcorp.com/img/media/_RodrickswpUSletter.pdf)

No assessment can be completed without the imposition of certain assumptions

that do not have complete

scientific substantiation. There is a clear danger, the Red Book authors

announced, that assessments can be manipulated by the assessor (whether under

the influence of the risk manager or not), to select, on a case by- case basis,

those assumptions that will guarantee a desired outcome.

This question of institutional separation arose because of allegations that

risk assessment outcomes could be easily manipulated to meet the predetermined

desires of regulators—to regulate or not to regulate, depending upon the

political climate and other factors unrelated to public health. Institutional

separation of the scientific activities of regulators from those of the policy

makers should help to purify those activities, or so some thought.

These various regulatory efforts of the late 1970’s were met with much

skepticism. Some declared that the “no safe level†principle for carcinogens

was

inviolate, and that risk-based approaches threatened that principle and

weakened public health protection (NRC, 1983).

Once a substance was identified as a carcinogen, factors other than the risk

it posed dictated the Permissible Exposure Limit (PEL). In its effort to

regulate benzene under the approach, the agency was challenged by the American

Petroleum Institute, and the case rose to the US Supreme Court. The Court

directed OSHA to incorporate quantitative risk assessments into its regulatory

efforts on carcinogens, and required the agency to demonstrate that a

significant risk of carcinogenicity existed at the current PEL, and that a

significant

reduction in risk would occur if a new and lower PEL were instituted. How

could a new PEL be justified, the Court reasoned, unless it provided

significant health benefits—i.e., risk reductions. The Court explicitly

recognized the

significant uncertainties associated with the risk assessment process, but

held that OSHA had to do the best it could (Merrill, 2003). OSHA has followed

this approach ever since (although most of its efforts on workplace

carcinogens took place before the 1990’s, and the agency has not been

particularly

active in this area since that time).

At the

time no known chemical had produced malignancies in animals at doses as low

as those at which aflatoxins

(B1 in particular) were active; even today it is surpassed in this respect

only by 2,3,7,8-tetrachloro(B1 in pa

dioxin. (A most informative exercise involves comparing and contrasting this

pair of extraordinarily potent

carcinogens, which otherwise differ in so many ways).

Convincing evidence of carcinogenicity

coupled with certain knowledge that people were being exposed, on a

worldwide and regular basis at

doses that were not obviously trivial, placed these naturally occurring

compounds squarely under the public

health spotlight

Armitage and Doll, 1954.

Hutt proposed that “safe doses†for carcinogens such

as DES could be defined as those associated with lifetime risk levels of

less than one-in-one million, when

those risks were estimated using a linear, no-threshold model (several

publications had demonstrated that

the Mantel- approach could not be counted on to place an upper bound on

risk at low doses but that

a linear, no-threshold model could).

Although it was estimated in a different way than that proposed by Mantel

and , their “virtually safe

dose†became Hutt’s “safe dose†(FDA, he used to say, did not

permit

doses for added carcinogens

that were only “virtually†safe). The selection of a lifetime risk level

considered sufficiently low to define a safe dose was not a scientific, but

rather a policy decision.

Kenny Crump published his so-called “linearized†multistage model for

low-dose extrapolation in 1976, and the EPA officially adopted it (IRLG, 1979;

EPA, 1986). In doing so, the agency had to find a way to deal with the

proliferation of statistically and biologically based models proposed for

low-dose

extrapolation that was seen in the scientific literature during the 1975-1980

period (NRC, 1983). None could be demonstrated to yield an accurate estimate of

low-dose risk, and it could be readily seen that the models under discussion

could yield very large differences in low-dose risks for the same carcinogen

at the same dose.

There was no way to resolve this problem without making a choice among

models that was not based on purely scientific understanding.

The very small risks estimated by these methods are, in fact, generally

unverifiable by any existing epidemiological method (IRLG, 1979, Rodricks,

2006).

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