The extent of the risk is, at present, only dimly perceivable. For one thing, most laboratory
studies have been relatively short-term efforts that involved exposure to the test system for days or
weeks, but rarely longer. Human exposure in the environment is obviously longer-term, and the present
laboratory studies can only provide an inkling of the true consequences. Another point is that the
laboratory studies have usually involved only one frequency or field in contrast to environmental EMFs
which consist of a superimposition of many frequencies and fields, and the possibility of a synergistic
interaction in the environment is virtually unexplored.
As we have shown, the biological concept of stress affords the most useful approach to the
analysis of bioeffects caused by EMFs. Applied to environmental exposure, the stress hypothesis leads
to the conclusion that the disease or effect produced in exposed subjects will depend on the genetic
predisposition and previous history of each subject, as well as on the electrical characteristics of the
EMF and the conditions of exposure. Thus, epidemiological studies would be expected to show a
correlation between environmental EMFs and a broad class of ills, rather than a specific disease,
because that is the expected result in an animal population chronically subjected to any stressor. This is
precisely what has been found in the epidemiological studies and surveys. Associations have been
reported between environmental EMFs and diverse phenomena including cancer, suicide, and
cardiovascular function. In the occupational setting, a disease syndrome has been identified in
individuals exposed to EMFs that leads to a clinically diagnosable state of biological stress, and to
specific effects such as cataracts and, apparently, changes in human reproduction.
What is the appropriate basis upon which to regulate environmental EMFs? Recently, the Public
Service Commission of West Virginia in approving construction of a high-voltage power line with no
provision for protection of the public from the electric and magnetic fields, reasoned that there were no
known biological effects of such fields in people who were regularly exposed to similar fields of other
lines (68). This finding, while technically correct, is hardly surprising because there have been no
studies of the health consequences of such chronically exposed subjects. Under this regulatory
approach-known as the dead-body theory-the regulator demands legal evidence of actual harm to
exposed subjects. The absence of such evidence-for whatever reason-is construed against the interests
of the exposed subjects, usually product users of local land-owners. We think that this approach is
wrong because it is both unfair and unethical. EMF-producing industries, which have resources to
support epidemiological studies but have failed to do so, should not be allowed to shift the onus to the
consumer or local landowner who is in no position at all to supply such proof. The dead-body
approach, moreover, wrongly presupposes the acceptability of using human beings in an involuntary
program of damage assessment of EMF levels known to be biologically active from laboratory studies.
Federally-supported investigators in the U.S. cannot lawfully and ethically apply, for example, 10 µW
or 500 v/m or 0.5 gauss to human subjects in a laboratory study without first following all the rules and
safeguards attendant to human experimentation protocols. It seems grossly inconsistent, therefore, for
private industrial groups, and others, to do so.
Risk-evaluation is an alternative, and we suggest much superior, approach to the regulation of
environmental EMFs. Here the regulatory agency focuses on the laboratory studies and tries to
determine their relevance to the particular health-and-safety evaluation at hand, and the degree of risk
that may permissibly be imputed to the human-exposure situation. It asks: was the strength and
frequency used in the laboratory comparable to that which will be produced by the hardware under
consideration? How does the duration of laboratory exposure compare to the normal patterns of human
exposure that will occur? What was the test species? (Clearly results from monkeys merit more weight
than those obtained from bean plants.) Was the optimum species used for the particular physiological
characteristic monitored? (The pig, for example, in studies of skin-healing, or the rabbit for studies of
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