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ous to your health if a single bee is ever detected. I will leave it to your imagi-
nation on modern science s ability to detect insects. These types of laws, as
illustrated in earlier chapters, now equate detection of a hazard to a calcula-
ble risk. I will also not discuss the adverse effects of bee elimination, such as
lack of pollination.
What is the real point of presenting this silly analogy? First there are
numerous safeguards built into our regulatory system to compensate for sci-
entific uncertainty and variability. These take a hard piece of experimental
data and offer a safety cushion in case the trials were designed wrong or a sen-
sitive population should be considered. This actual process, as applied to
fruits and vegetables, is fully outlined in Appendix A. The numbers that result
from this process are scientifically reasonable. However, many regulations
now make the ultraconservative assumption that even one molecule of a
chemical, which at lifetime exposures to high doses could induce cancer in a
laboratory animal, might be hazardous based on detection rather than real
risk. Any level is prohibited. The reader should recall the paradox of applying
this to the natural constituents of food.
RISK AND REGULATIONS 87
The subtle effect of changing endpoints by adopting detection rather than the safe
level of a chemical is rarely communicated to the public, and thus exposure is equat-
ed to a real risk. In fact, a number of public panics have been started just by detec-
tion of a chemical without any assessment of risk!
As the bees are buzzing a few feet from my deck chair, I question why am I
not attacked? Probably the bees are more interested in the nectar of flowers
than in stinging me. This is where the exposure in the risk equation must be
incorporated. This was previously presented as risk = hazard exposure.
The bee next to me remains just as hazardous as if it were sitting on my arm
ready to sting. The difference is that with so many flowers growing in my yard
and with the location of my jacket between the bee and my skin, I have addi-
tional protection drastically reducing my potential exposure. The bee and its
hazard doesn t change, but the bee s access to me does, which lowers exposure
and thus risk.
The same argument holds for exposure to a known carcinogen.
Theoretically, one molecule of a carcinogen could mutate a specific piece of
DNA (for example, a p53 tumor-suppression gene) in my body and cause a
normal cell to become transformed to a cancerous cell. This cell could then
undergo clonal expansion, evade detection by my immune system, and form
a tumor. However, just as it is unlikely that the bee will sting me, it is equally
unlikely that this single cancer-causing molecule will be absorbed into my
body and cause an effect. Absorption by any route would require a high con-
centration of the molecules to be present, thus forcing the molecules to dif-
fuse into the body. A single molecule cannot provide this driving force. It must
then evade metabolism by my body s protective mechanisms and circulate
through my blood and body until a susceptible cell is found. Using my bee
analogy, the bee must first find and land on me before I slap it or spray it. One
bee will not intimidate me, but a hive will. Similarly, although large doses of
a chemical may cause harm, low doses may not. The analogies are endless.
Crossing a street blindfolded may not be harmful on a deserted expressway at
5 a.m., but it is suicide on the same road during the 5 p.m. rush hour. This is
the crux of the dose-response relationship. Also, if I am protected, it is unlike-
ly harm will come. The same holds for chemical toxicity because our bodies
have developed exquisite and very efficient protective mechanisms. Food,
even with theoretically and experimentally proven natural carcinogens, is
beneficial to our health. A hazard may always be present, but because of low
exposure, risk is minimal.
Other lessons may be learned from this analogy, such as the difficulty of
dealing with unusually sensitive or allergic individuals as well as environmen-
tal versus occupational exposure. The chances of bee stings dramatically
increase if one is a beekeeper. Precautions are taken to ensure that such indi-
viduals are protected, as there is a real risk. The same holds for pesticides.
88 CHAPTER 6
Applicators and manufacturers are exposed to high doses, so they must take
precautions. Otherwise the serious toxicity predicted by animal studies may
actually occur. One could argue that farmers are at an increased risk, howev-
er, (as discussed earlier) there is little epidemiological data to support this for
chronic toxicity. Their risk is similar to applicators for acute toxicity. A person
who is allergic to bees should not become a beekeeper. Does this mean, how-
ever, that beekeeping and flower gardens should be outlawed by the VIPA
because some individuals who are allergic to bees may be stung?
 Will you walk into my parlour? said a Spider to a Fly;
  Tis the prettiest little parlour that ever you did spy.
(Mary Howitt,  The Spider and the Fly )
New laws are constantly being passed and our understanding of science [ Pobierz całość w formacie PDF ]
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