Title: Water Pollution, Pesticide Residues, and Cancer
Full Citation
Permanent Link: http://ufdc.ufl.edu/WL00001452/00001
 Material Information
Title: Water Pollution, Pesticide Residues, and Cancer
Physical Description: Book
Language: English
Publisher: NAWC Water
Spatial Coverage: North America -- United States of America -- Florida
Abstract: Water Pollution, Pesticide Residues, and Cancer, Summer 1986, Volume 27, No. 2
General Note: Box 8, Folder 5 ( Vail Conference, 1995 - 1995 ), Item 66
Funding: Digitized by the Legal Technology Institute in the Levin College of Law at the University of Florida.
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Bibliographic ID: WL00001452
Volume ID: VID00001
Source Institution: Levin College of Law, University of Florida
Holding Location: Levin College of Law, University of Florida
Rights Management: All rights reserved by the source institution and holding location.

Full Text

WATER, Vol. 27, Number 2 (Summer 1986)

S t.i i- _- .7 7 -

Adopted from November 11, 1985, Testimony of Professor Bruce N. Ames to Art Torres, Californio
Senate Committee on Toxics and Public Safety Monogement

The carcinogens and pesticide residues
currently being found in California water
supplies, such as in Silicon Valley, are
present in extraordinarily tiny amounts
that, except in rare cases, are trivial rel-
ative to the background level of carcino-
gens in Nature. Therefore, I am convinced
that such water pollution is irrelevant as
a cause of human cancer.
The main current fallacy in our approach
to such pollution consists in believing that
carcinogens are rare and that they are mostly
man-made chemicals. Quite the contrary
(0f the case. My estimate is that over 99.99%
of the carcinogens Californians ingest are
from natural (e.g., substances normally
present in food) or traditional sources (e.g.,

cigarettes, alcohol, and chemicals formed
by cooking food).
Every meal has many carcinogens and
when one compares the level of carcino-
gens in contaminated water or pesticide
residues in food to the level of natural
carcinogens also present in the diet, it is
clear that water pollution or pesticide res-
idues represent a trivial exposure by com-
Water pollution and pesticide residues
are almost always present in the ppb (parts
per billion) range. One part per billion
(i.e., 1 person in all of China) is an
extraordinarily small amount. By compar-
ison, the carcinogens in a few common
drinks are listed below. Every common

drink contains carcinogens.
a) Coffee contains the known natural
carcinogens hydrogen peroxide and meth-
ylglyoxal, each at about 4,000 ppb. b) Tap
water contains the carcinogen chloroform
at 83 ppb (U.S. average), as a conse-
quence of chlorinating the water, c) Cola
drinks contain the carcinogen formalde-
hyde at 7,900 ppb, though this is not much
higher than human blood, which averages
about 3,000 ppb in formaldehyde from
normal metabolism. d) Beer contains
nitrosamines, formaldehyde (700 ppb), and
alcohol (50 million ppb, or 5%), all known
carcinogens. Alcohol consumption is a
known cause of human cancer (3% of U.S.
(continued next page)




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CANCER, continued

cancer) and ethyl alcohol is a carcinogen
in rats. e) Milk contains a high percentage
of fat, and high fat consumption has been
implicated in human breast and colon can-
cer and rodent cancer (though milk is an
important source of calcium, which may
be important as an anticarcinogen). And
f) fruit juices may have various amounts
of carcinogenic mold toxins, depending
on how many moldy fruits were processed.
Calculating a possible hazard to humans
from information obtained from a cancer
test on rats must take into account the
potency of the carcinogen in rats as well
as the human dose. We are just completing
a study where we compare possible hazards
for humans due to typical daily intake of
carcinogens, adjusting for the potency of
each carcinogen from the animal data.
This adjustment is necessary because the
potency of carcinogens varies over a mil-
lion-fold, e.g., aflatoxin, a mold carcin-
ogen that is present in small amounts in
peanut butter (2 ppb U.S. average) or in
corn products such as tortillas, requires
about a million times smaller dose to cause
Q4 he same incidence of cancer in test ani-
Smals as trichloroethylene, which was the
main contaminant in Silicon Valley wells.
I give some comparisons below.
Contaminated water. The level of car-
cinogens in contaminated well water (e.g.,
trichloroethylene in Silicon Valley or
Woburn, Massachusetts) only rarely
involves a possible hazard more than that
of ordinary chlorinated tap water. Of 35
private wells shut down in Silicon Valley
because of their supposed carcinogenic
hazard in an EPA study, only two were of
greater possible hazard than ordinary tap
water (well water usually lacks the chlo-
roform present in chlorinated tap water),
and the most polluted well (2,800 ppb
trichloroethylene) is still at least 1,000
times less of a possible hazard than an equal
volume of cola, beer, or wine. This is
because trichloroethylene is an extremely
weak carcinogen. It is comparable to sac-
charin and only 10 times more potent than
alcohol, which is present at about 50 mil-
lion ppb in a beer. Given that the con-
,-umption of tap water is only about 1 or
i liters per day, it seems unlikely that man-
made water pollution in the trace amounts
typically seen is causing more than a min-
imal hazard.

Pesticide residues. Man-made pesticide
residues present in our food amount to
about 100 ppb on the average; most of
these residues are composed of non-car-
cinogenic compounds. The man-made
carcinogenic residue of most interest in
food is likely to be DDT and its metabolite
DDE. The possible hazard of the DDT/
DDE of the average U.S. daily intake is
equivalent to that of the chloroform in 1
glass of tap water and is insignificant com-
pared to natural carcinogens in our diet.
Even an occasional highly DDT/DDE- or
PCB-contaminated fish (e.g., 100 times
the average level) would contribute a pos-
sible hazard that is comparable to the aver-
age peanut butter sandwich and is small
compared to other very common minimal
risks such as a glass of beer.
Nature's pesticides. We are ingesting nat-
ural pesticides in our diet in amounts at
least 10,000 times more than man-made
pesticide residues. Natural pesticides are
natural toxic chemicals, which are present
in all plants, usually making up 5-10% of
a plant's weight. They have an enormous
variety of chemical structures, though only
a few are present in each plant species.
Their function is protection against fungi,
insects and animal predators. Thus, a major
aspect of evolution of plants is chemical
warfare. There has been relatively little
research in the toxicology or carcinogen-
icity of these compounds until quite
recently, and so, very few of the large
number present in the human diet have
been tested in animal cancer bioassays. A
fair percentage of those few that have been
tested have turned out to be carcinogens
in rats or mice. They include estragole (in
basil), safrole (in herbs), symphitine (in
comfrey tea), psoralens (in pars, and
celery), hydrazines (in mushrooms), and
allyl isothiocyanate (in mustard). The
possible carcinogenic hazard of Nature's
pesticides completely overshadow the traces
of man-made pesticide residues found in
the daily diet. Plants also contain anti-
carcinogens and valuable nutrients, so I
believe that even these possible hazards
seem too small to worry about, particularly
given the points made below.

Skepticism about extrapolating risks from
rodents. All calculations of human risk based
on rat and mouse cancer tests, both from
natural and man-made carcinogens, are
hypothetical. Thus, they should be taken

with a great dose of skepticism, unlike
known human carcinogens such as smok-
ing (400,000 deaths from cancer, heart
disease, etc., per year in the U.S.) or
alcoholic beverages (100,000 deaths from
cancer, etc. per year). There are many new
reasons for being skeptical of uncritical
low-dose extrapolation of risk to humans
from animal data obtained by feeding
enormous doses, which can't be discussed
here. This is reinforced by the studies of
cancer epidemiologists who are making
considerable progress in understanding the
smoking, dietary, hormonal, viral, and
occupational contributions to human can-
cer, but who are finding remarkably little
solid evidence for any significant contri-
bution from pollution.
Since we now know that carcinogens
are common, not rare (over half of the
chemicals tested in rats or mice were judged
carcinogens), we must of necessity ignore
the trivia if we wish to deal with the impor-
tant causes of cancer. We might possibly
eliminate every trace of man-made car-
cinogen from our water or food supply, but
it would cost an enormous amount of Cal-
ifornia's wealth, be of minimal relevance
to causes of human cancer, and distract
health workers from real, more important
risks. Thus, one can either chase after
parts per billion of every man-made car-
cinogen that turns up or have some sen-
sible regulations about pollution. We should
also remember that, except for the increase
in cancer due to smoking, age-adjusted
cancer death rates are decreasing (stom-
ach, uterus, liver) or have not increased,
and that life expectancy increases every
year. a

Professor Ames-is Chairman of the
Department of Biochemistr University
of California, Berkeley, and was formerly
on the Board of Directors of the National
Cancer Institute (National Cancer Advi-
sory Board). He is a memberofthe National
Academy of Sciences. He was the recipient
of the most prestigious award for cancer
research, the General Motors Cancer
Research Foundation Prize (1983), and
of the highest award in environmental
achievement, the Tyler Prize (1985). He
does no consulting for the chemical, drug,
or food industry, or for law firs.



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