By Steven B. Oppenheimer
r in
Humanaam de
vs r1 t ra� f od carcin
ens
ns:
WHICH POSE THE GREATEST CANCER RISK?
Human-made chemicals
HERE HAS BEEN widespread belief that air, wa­
ter, and food pollution by human-made chem­
icals plays a major role in cancer-caused
deaths in the United States. The sort of evidence to
support this contention comes mainly from epi­
demiological studies examining cancer rates in vari­
ous sections of the nation and in various occupa­
tional groupings.•-'
Human-made chem icals are clearly responsible
for numerous cancer deaths among workers in hi gh
risk occupations. •,s-J Some studies, however, sug.:
gest that only about 4�o of cancers are directly re­
lated to occupational exposure. 8
What about those remaining? Smoking and the
use of tobacco appears responsible for about 30117o
environmental and medical exposure to radiatio
I OJo, alcohol 4�o, sexual practices (probably viral
transmission) 7%, heredity 2%, food additives 1 0Jll
viruses and infections JOOJo, unknown factors a
least 5%, environmental pollution (not occupa­
tional) 2o/o, and diet about 30�o. �
The two latter factors are probably a surprise to
many readers. That is, environmental pollution ap­
pears to be a rather minor cause of cancer while diet
is a major cause. The general attitude that industry
is responsible for most of our cancer woes does not
seem to be sup�orted by many studies, although
some experts bebeve that human-made pollution is
responsible for far more than the 407o-8% of can­
cers listed above. 9 An interesting statistic that can
be used to illustrate the point about human-made
pollution vs other factors is that one would have t o
breathe Los Angeles smog for one year to equal the
amount of combustion products inhaled in one day
of smoking. 10
T
�
�
Dr. Oppenheimer is Statewide Trustees Outstanding Professor,
Department of Biology, California State University. He is
'J'!lomas Eckstrom Fel/o win Cancer Biology and Principal In ves1/gator for the National Science Foundation and the National
Cancer lnstitute, and Director of the Centerfor Cancer and De­
veloprnemal Biology.
16
FEBRUARY 1985
Although there is some controversy concerning
the numbers of cancers resulting from environmen­
tal pollution in the general population, there is
strong agreement that carcinogen exposure in vari­
ous high risk occupations is a major cause of cancer
in these occupations and that much.more regulation
of these carcinogens is needed. 9• '0
The diet controversy
Since the appearance of the National Research
Council's Report on Diet, Nutrition and Cancer''
and Bruce Ames's arHcle, "Dietary Carcinogens
and Anticarcinogens, '112 there has been a virtual de­
luge of articles, papers, and actions by agencies
such as the National Cancer Institute and American
Cancer Society stressing the importance of diet in
the etiology and prevention of cancer. The dust is
beginning to settle, and the remainder of this article
will attempt to separate fact from fiction with re­
spect to the potentially immensely important topic
of cancer and diet.
Natural food toxins
Bruce Ames's paper'1 and the National Research
Council's Report'' present two basic sorts of find­
ings. One type of finding, which can be considered
hard data, is that certain substances found in foods
are definitely carcinogenic in animals. The other
sort of finding, based on epidemiological studies, is
that people who eat certain foods appear to be more
or less likely to develop certain cancers. These are
soft data.
That a specific agent is carcinogenic in animals is
not difficult to prove. It is much more difficult to
prove, however, that a group of people who eat cer­
tain foods rich in certain agents have either in­
creased or decreased cancer rates because of the
specific suspect agents.
A review of the hard data will now be presented
followed by an examination of why the other d a t
�
CARCINOGENS continued
are really soft. There is widespread acceptance of
the principle of animal tests as being a valid method
for determining the likely carcinogenicity of sub­
stances.1 The following foods contain substances
that are known carcinogens or likely human car­
cinogens based upon animal testing.'' Many of
these agents are naturally occurring plant poisons
that have evolved over millions of years to aid in
protection of the plants from insect attack, mold
growth, and invasi on by other microorganisms. 12
The specific problem agent is given in parentheses
beside each food.
Crude cottonseed oil (gossypol)
Black pepper (safrole, piperine)
Mushrooms (hydrazines)
Celery, parsnips, figs, parsley {psoralen deriva­
tives)
Horseradish, oil of mustard (allyl isothiocyanate)
Smoked, browned, and burnt foods including
coffee (combustion products similar to those in
cigarette smoke)
Moldy foods (aflatoxins, sterigmatocystin)
Thus, as is the case for numerous occupational car­
cinogens, these food items contain agents that have
been found to be likely carcinogens in animals.
What appears to be critically important to the gen­
eral population is that reliable estimates suggest
that individuals consume 10,000 times more of
these natural food toxins than human-made ones.'1
In terms of quantity, therefore, there is good reason
to believe that natural food carcinogens might be a
major cause of cancer in the general population.' 2
Fats, fiber, and vitamins
Studies reported in the National Research Coun­
cil's report on Diet, Nutrition and Cancer'' and
Bruce Ames's article on dietary carcinogens and
anticarcinogens12 show correlations between high
fat intake and increased rates of colon, breast, and
'
prostate cancers. •11• '2 Colon cancer risk appears
somewhat related to low fiber consumption, and
some studies suggest that very low levels of vitamin
A are associated with increased risk of lung and
12
bladder cancers.'•'' '
As mentioned earlier, the evidence in support of
these sorts of relationships is. generally correlation.
Specific population groups with low fat intake seem
to have low breast cancer rates, groups of people
who consume lots of fiber-rich foods have very low
colon cancer rates, and so on. In addition, the fact
that an individual group with an increased lung can­
cer rate has a low intake or serum level of vitamin A
proves nothing. There are .so many variables that
may not have been considered in such studies that at
present the evidence to support these notions is not
18
FEBRUARY 1985
convincing.9 In fact, numerous recent studies have
cast doubt upon some of the findings reported earl­
ier. Some studies do not show correlations between
intake of speCific vitamins and cancer risk and even
the rather substantial body of data on the relation­
ship of fat intake and cancer is open to question.'
Is there enough reliable evidence to propose to
the general public that it should modify its diet to
reduce consumption of fats and that it should in­
crease consumption of fiber-rich foods and fruits
and vegetables, particularly those rich in vitamin A,
beta carotene, and vitamin C? Although these pro­
posals are based upon soft data, enough suggestive
information is on hand to justify acting now. This
conclusion is based upon the following facts.
1. It will probably take decades to determine
clearly if these actions definitely prevent human
cancers. Even if some of them do not prevent can­
cer, there is little doubt that a diet low in fat and
high in fiber reduces the risk of cardiovascular dis­
ease and diverticulitis and decreases intake of fat­
soluble synthetic carcinogenic contaminants. 9
2. Colon-rectum cancer accounts for about
50,000 deaths per year, while breast and prostate
cancers account for about 40,000 and 24,000
deaths, respectively, in the United States.2 These
cancers, along with lung cancers, primarily caused
by smoking, account for over 500Jo of the cancer
deaths in this nation. Although some lung cancers
result from occupational or environmental expo­
sure to other carcinogens, most clearly result from
smoking. Lung cancers, and other smoking-related
cancers, are therefore preventable. Colon-rectum
cancer and breast cancers, on the other hand, have
not been definitively tied to any major known car­
cinogen exposure that affects large population
groups. 2•1 Especially in the case of colon-rectum
cancer, which, next to lung cancer, kills the most
people each year in the United States, a dietary
etiology is likely. 1•3 The epithelial lining of t h e
colon and rectum is constantly exposed t o a variety
of carcinogens, most of which are derived from the
diet or from breakdown products of substa n ce s
originating in the dieV This theoretical argument,
coupled with epidemiological correlations with re­
spect to fat consumption and the knowledge that fat
breakdown products can be carcinogenic, 3•11• '2 sup­
ports the notion that enough information is avail­
able for immediate action.
3. Numerous experimental studies show that vita­
mins A, C, and E inhibit a variety of chemically in­
duced cancers at a variety of anatomical sites 1•3, 7 •13
in animals, and thatvitamins C and E block forma­
tion of some carcinogens and mutagens in the hu­
man intestine.'•3•7 In addition, these vitamins are
antioxidants, blocking oxidation reactions that may
be involved in carcinogenesis, 3• 12 and some studies
show correlations between increased intake of these
agents and reduced cancer risk. 1 3 11 12 Therefore,
•
•
•
on the basis of evidence from various disciplines,
there is good reason for the public to increase con­
sumption of foods rich in antioxidant vitamins at
this time.
Conclusions
Although human-made chemicals are responsible
for numerous occupationally related cancer deaths,
there is no good evidence to suggest that most can­
cer deaths are caused by such agents in the general
public. 8• '2 Diet, on the other hand, is a likely cause
of colon-rectum cancer, breast cancer, and prostate
cancer, among others; and because these cancers ac­
count for a very large number of cancer deaths, diet
should be of major concern to the general public.
Upon examination of hard vs. soft data in the
diet arena, it can be reasonably concluded that
some foods should be avoided because they contain
known carcinogens, 1• 12 while other foods should
become part of the regular diet because they inhibit
carcinogenesis. Evidence from a variety of scientific
disciplines supports these actions, even if all the in­
formation is not yet available. 1• 10-12
References
I.
OPPENHEIMER, S.B., Cancer Prevention Guidebook (Bur­
gess, Minneapolis, 1984).
2. American Cancer Society, Cancer Facts and Figures (I 984).
3. OPPENHEIMER, S.B., Cancer: A Biological and Clinical In­
troduction (Allyn and Bacon, Boston, 1982).
4. New York Academy of Sciences, Cancer and the Worker
(1977).
5. SCHOTTENFELD, D. and HAAS, J.F., "Carcinogens in tl1e
workplace," Ca- A Cancer}. Clin. 29, 144 (1979).
6.
WILLIAMS, R.R., STEGENS, N.L. and GOLDSMITH, J.R.,
"Associations of cancer site and type witn occupation and
industry from the Third National Cancer Survey interview,"
J. Nat. Cancer Ins/. 59, 1147 (1977).
7.
OPPENHEIMER, S.B., "Prevention of cancer," Am. Lab. 15
(2) 66 (1983).
8. DOLL, R. and PETO, R., The CausesofCancer(Oxford, New
York, 1981).
9. EPSTEIN, s.s. and SWARTZ, J.B., "Letter on cancer and
diet," Science 224, 658 (1984).
10. AMES, B.N., "Letter on cancer and diet," Science 224, 658
(1984).
II. National Research Council, "Report on diet, nutrition and
cancer" (National Academy of Sciences,
1982).
Washington,
12. AMES, B.N., "Dietary carcinogens and anticarcinogens,"
Science 221, 1256 (1983).
13. SPORN, M.B., "Combination chemoprevention of cancer,"
Nature 287, 107 (1980).
Circle Reader Service Card No. 20
llf"OO
1Q