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Epidemiological principles for EMF and EMR studies - Lincoln ...

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3<br />

a cotton mill were chronically exposed to dust <strong>and</strong> fibre <strong>and</strong> showed elevated rates<br />

of respiratory disease. The disease rates were consistently elevated about three<br />

times higher than average, but never significantly. The evidence was strong<br />

enough that it was concluded that it was a causal effect because "The evidence<br />

was so clear cut", Hill (1965). Sir Austin addresses the question of statistical<br />

significance in the assessment of a causal relationship. He states in relation to the<br />

question of causation:<br />

“No <strong>for</strong>mal tests of significance can answer these questions. Such tests can, <strong>and</strong><br />

should, remind us of the effects that the play of chance can create, <strong>and</strong> they will<br />

instruct us in the likely magnitude of those effects. Beyond that they contribute<br />

nothing to the ‘proof’ of the hypothesis.”<br />

Again, modern epidemiology often uses the term “criteria” <strong>for</strong> the Brad<strong>for</strong>d Hill<br />

viewpoints. This is treating this approach as a sine qua non, directly contrary to Sir<br />

Austin’s strong statement. I believe that this is placing the public <strong>and</strong> workers at<br />

much higher risk levels by significantly raising the level of evidence thresholds <strong>for</strong><br />

deciding about causal effects. This results in setting public health protection<br />

st<strong>and</strong>ards that allow exposures at levels that are extremely significantly higher than<br />

those which have been shown to cause serious health effects found from multiple<br />

independent epidemiological <strong>studies</strong>.<br />

Third <strong>Epidemiological</strong> Principle:<br />

Association to Causation - the Brad<strong>for</strong>d Hill Approach:<br />

To deal with the question of whether there is a causal relationship Sir Austin gives<br />

us “Here then are nine different viewpoints from all of which we should study<br />

association be<strong>for</strong>e we cry causation. What I do not believe - <strong>and</strong> this has been<br />

suggested - is that we can usefully lay down some hard-<strong>and</strong>-fast rules of evidence<br />

that must be obeyed be<strong>for</strong>e we accept cause-<strong>and</strong>-effect. None of my nine<br />

viewpoints can bring indisputable evidence <strong>for</strong> or against the cause-<strong>and</strong>-effect<br />

hypothesis <strong>and</strong> none can be required as a sine qua non [essential requirement].<br />

What they can do, with greater or less strength, is help us to make up our minds on<br />

the fundamental question – it is to any other way of explaining the set of facts<br />

be<strong>for</strong>e us, is there any other answer equally or more likely, than cause <strong>and</strong> effect?”<br />

Sir Austin Brad<strong>for</strong>d Hill provides a well-established <strong>and</strong> very sensible health<br />

protection approach to the assessment of the available evidence of association to<br />

causation of human exposure to a disease agent <strong>and</strong> illness. Sir Austin’s approach<br />

has commonly been applied to the assessment of the effects of chemicals.<br />

Sir Austin Brad<strong>for</strong>d Hill set out his nine viewpoints as (1) Strength; (2)<br />

Consistency; (3) Specificity; (4) Temporality; (5) Biological Gradient; (6)<br />

Plausibility; (7) Coherence; (8) Experiment <strong>and</strong> (9) Analogy, Hill (1965).<br />

Sir Austin discusses each of his viewpoints <strong>and</strong> gives examples to clarify the<br />

context of how the assessment was being considered. Only one, temporality, is<br />

essential because the exposure must take place be<strong>for</strong>e it can be associated with

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