Diane Relf
Virginia Cooperative Extension
Think
about the word "carcinogen." What pops into your
mind? Pesticides? Smoking? Asbestos? Pesto? There probably
aren't too many people who actually thought "pesto,"
but it would fit into the category. Basil, the primary ingredient
of pesto, is loaded with estragole, which is responsible for
that unforgettable flavor and is a rodent carcinogen.
Surprised?
Well, hold onto your seat, basil is just the beginning. Mustard
contains allyl isothiocyanate; comfrey contains symphytine;
and mushrooms contain various hydrazines, all of which are
carcinogens with higher potencies in rats or mice than poly-chlorinated
biphenyls (PCBs). It seems that virtually every plant contains
natural compounds that act as protection against insects,
microorganisms, and herbivores. About half of these compounds
tested so far have proven to be carcinogenic, at least in
rats or mice. And we eat about 10,000 times the amount by
weight of these natural pesticides as we do synthetic pesticide
residues.
There
are many other naturally occurring sources of carcinogens
in our daily lives. Many carcinogens are created during cooking.
Charred meat, browned bread crusts, and fermented products
are major sources of carcinogens in the diet. Our body's own
metabolism is responsible for releasing carcinogenic oxygen
radicals. The large number of naturally occurring carcinogens
is likely to overwhelm any effect from the small amounts of
synthetic pesticides we consume. While this doesn't mean that
cancer risks from synthetic pesticide residues should be ignored,
it does put them into perspective. Is it necessary to panic
about a trace amount of ethylene dibromide (an agricultural
fumigant) when the pesto packs a stronger punch?
Another
thing to remember is that when we consume synthetic pesticide
residues and natural pesticides, we generally consume them
on or in fruits and vegetables. Fruits and vegetables also
contain anti-carcinogens, including vitamins E and C and beta-carotene.
These anti-carcinogens, combined with your body's defenses,
protect against both natural and synthetic carcinogens.
Of course,
it makes sense to eliminate the largest risks from one's diet
and environment. To do that, some measure of carcinogenicity
is necessary. Unfortunately, most of the data is for rodent,
not human, carcinogens. In fact, it is impossible to calculate
human risk based on a rodent exposure, but we may be guided
in our decisions by rodent data. Prudence would dictate limiting
those substances that are highly potent rodent carcinogens.
Bruce
Ames of the University of California and his colleagues have
developed a scale for comparing carcinogens based on human
exposure and rodent carcinogenicity. While this scale does
not allow for actually calculating risk, it does serve to
point out compounds that may be of greater concern than others.
The greater the human exposure to the rodent carcinogen or
the greater the potency of the carcinogen in rodents, the
higher the human exposure/rodent potency ratio (HERP).
HERP |
Daily human exposure percentage |
140
|
EDB: workers' daily intake, high exposure
|
5.8
|
Formaldehyde: workers' average daily intake
|
6.2
|
Comfrey-pepsin tablets (9 daily), from comfrey root
|
2.8
|
Beer (12 ounces) from ethyl alcohol
|
0.1
|
Mushroom, one raw (15 g) from hydrazines
|
0.1
|
Basil (1 g of dried leaf) from estragole
|
0.07
|
Brown mustard (5 g), from allyl isothiocyanate
|
0.03
|
Peanut butter (32 g, one sandwich) from aflatoxin content of 64 mg
|
0.03
|
Comfrey herb tea, 1 cup
|
0.003
|
Bacon, cooked (100 g)
|
0.0004
|
EDB: daily dietary intake, U.S. average
|
0.0003
|
DDE/DDT: daily dietary intake, U.S. average
|
0.0002
|
PCBs: daily dietary intake, U.S. average
|
2.1
|
Mobile home air (14 hours/day)
|
0.6
|
Conventional home air (14 hours/day) |
Looking
at this data, one can see that a can of beer exposes you to
a larger amount (based on body weight) of a rodent carcinogen
than does your average intake of PCBs, DDE/DDT, and ethylene
dibromide combined. The formaldehyde in conventional and mobile
home air results in much higher HERP's than do the chemical
residues listed.
Remember,
it is impossible to say, based on the data available, that
a synthetic pesticide is more or less likely to cause cancer
than a natural pesticide. The lower exposure rates as seen
in Table 1 suggest less of a risk from synthetic pesticide
residue, but don't prove it. It does seem reasonable to conclude
that occupational exposures to high concentrations of synthetic
chemicals and indoor air pollution may be a much greater risk
than either natural or synthetic pesticides in the diet.
It appears
that we continually are bombarded by carcinogens in our diet
and have been for all of our history. Remembering this may
help us keep our perspective on the carcinogenicity of pesticide
residues, especially when there is much that could be done
to reduce major sources of cancers, such as smoking and occupational
exposure. Relatively speaking, pesticide residue is a minor
cause of cancer and may even be irrelevant when considering
the vast number of natural pesticides with similar or greater
potencies.
Reference:
Ames, B.N., R. Magaw, and L. Gold. Ranking Possible Carcinogenic
Hazards. Science 236:271-80.
Disclaimer
and Reproduction Information: Information in NASD does not represent
NIOSH policy. Information included in NASD appears by permission
of the author and/or copyright holder. More
NASD Review: 04/2002
Diane
Relf, Extension Specialist, Environmental Horticulture
(Originally published as "Cancer Risks from Synthetic Pesticides
in Perspective," by Ellen M. Silva, Extension Technician,
Office of Consumer Horticulture, in The Virginia Gardener
Newsletter, Volume 9, Number 2.)
Posted April 1997
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