Paracelsus to Parascience:
The Environmental Cancer Distraction
by Bruce
N. Ames and Lois
Swirsky Gold
September 7, 1999
2. Even Rachel Carson Was Made of Chemicals: Natural Versus
Synthetic Chemicals
About 99.9% of the chemicals humans ingest are natural. The amounts of synthetic
pesticide residues in plant foods are insignificant compared to the amount of
natural pesticides produced by plants themselves [32-34]. Of all dietary pesticides
that humans eat, 99.99% are natural: they are chemicals produced by plants to
defend themselves against fungi, insects, and other animal predators [32-34].
Each plant produces a different array of such chemicals.
We have estimated that on average Americans ingest roughly 5,000 to 10,000
different natural pesticides and their breakdown products. Americans eat about
1,500 mg of natural pesticides per person per day, which is about 10,000 times
more than the 0.09 mg they consume of synthetic pesticide residues [33].
Even though only a small proportion of natural pesticides have been tested
for carcinogenicity, 37 of the 71 tested are rodent carcinogens. Naturally-occurring
pesticides that are rodent carcinogens are ubiquitous in fruits, vegetables, herbs,
and spices [34](Table 2).
Cooking foods produces about 2,000 mg per person per day of burnt material
that contains many rodent carcinogens and many mutagens. By contrast, the residues
of 200 synthetic chemicals measured by FDA, primarily synthetic pesticides, thought
to be of greatest importance, average only about 0.09 mg per person per day [33;34].
In a single cup of coffee the natural chemicals that are known rodent carcinogens
are about equal in weight to a year's worth of synthetic pesticide residues that
are rodent carcinogens, even though only 3% of the natural chemicals in roasted
coffee have been adequately tested for carcinogenicity [35](Table
3). This does not mean that coffee or natural pesticides are dangerous, but
rather that assumptions about high dose animal cancer tests for assessing human
risk at low doses need reexamination. No diet can be free of natural chemicals
that are rodent carcinogens [34].
Gaining a broad perspective about the vast number of chemicals to which humans
are exposed can be helpful when setting research and regulatory priorities [32;34-36].
Rodent cancer tests by themselves provide little information about how a chemical
causes cancer or about low-dose risk. The assumption that synthetic chemicals
are hazardous has led to a bias in testing, such that synthetic chemicals account
for 76% (451 of 590) of the chemicals tested chronically in both rats and mice
(Table 1). The natural world of chemicals has never been tested
systematically.
One reasonable strategy is to use a rough index to compare and rank possible
carcinogenic hazards from a wide variety of chemical exposures at levels that
humans typically receive, and then to focus on those that rank highest [1;3;35;37].
Ranking is a critical first step that can help to set priorities for selecting
chemicals for long term cancer tests, studies on mechanism, epidemiological research
and regulatory policy. Although one cannot say whether the ranked chemical exposures
are likely to be of major or minor importance in human cancer, it is not prudent
to focus attention on the possible hazards at the bottom of a ranking if, using
the same methodology to identify hazard, there are numerous, common human exposures
with much greater possible hazards. Our analyses are based on the HERP index (Human
Exposure/Rodent Potency), which indicates what percentage of the rodent carcinogenic
potency (dose to give half of the animals cancer) a human receives from a given
daily lifetime exposure [37]. A ranking based on standard linearized, regulatory
risk assessment would be similar.
Overall, our analyses have shown that HERP values for some historically high
exposures in the workplace (e.g., butadiene and tetrachloroethylene) and some
pharmaceuticals (e.g., clofibrate) rank high, and that there is an enormous background
of naturally-occurring rodent carcinogens in typical portions of common foods
that cast doubt on the relative importance of low-dose exposures to residues of
synthetic chemicals such as pesticides [1;3;35;37;38]. A committee of the National
Research Council of the National Academy of Sciences recently reached similar
conclusions about natural vs. synthetic chemicals in the diet, and called for
further research on natural chemicals [39].
The possible carcinogenic hazards from synthetic pesticides are minimal compared
to the background of nature's pesticides, though neither may be a hazard at the
low doses consumed. Analysis also indicates that many ordinary foods would not
pass the regulatory criteria used for synthetic chemicals. Caution is necessary
in drawing conclusions from the occurrence in the diet of natural chemicals that
are rodent carcinogens. It is not argued here that these dietary exposures are
necessarily of much relevance to human cancer. Data call for a reevaluation of
the utility of animal cancer tests in protecting the public against minor hypothetical
risks.
It is often assumed that because natural chemicals are part of human evolutionary
history, whereas synthetic chemicals are recent, the mechanisms that have evolved
in animals to cope with the toxicity of natural chemicals will fail to protect
against synthetic chemicals. This assumption is flawed for several reasons [32;40]:
1. Humans have many natural defenses that buffer against normal exposures to
toxins [32] and these are usually general, rather than tailored for each specific
chemical. Thus they work against both natural and synthetic chemicals. Examples
of general defenses include the continuous shedding of cells exposed to toxins
- the surface layers of the mouth, esophagus, stomach, intestine, colon, skin
and lungs are discarded every few days; DNA repair enzymes, which repair DNA that
was damaged from many different sources; and detoxification enzymes of the liver
and other organs which generally target classes of chemicals rather than individual
chemicals. That human defenses are usually general, rather than specific for each
chemical, makes good evolutionary sense. The reason that predators of plants evolved
general defenses is presumably to be prepared to counter a diverse and ever-changing
array of plant toxins in an evolving world; if a herbivore had defenses against
only a specific set of toxins, it would be at great disadvantage in obtaining
new food when favored foods became scarce or evolved new chemical defenses.
2. Various natural toxins, which have been present throughout vertebrate evolutionary
history, nevertheless cause cancer in vertebrates [32;37]. Mold toxins, such as
aflatoxin, have been shown to cause cancer in rodents and other species including
humans (Table 1). Many of the common elements are carcinogenic
to humans at high doses, e.g., salts of cadmium, beryllium, nickel, chromium and
arsenic, despite their presence throughout evolution. Furthermore, epidemiological
studies from various parts of the world show that certain natural chemicals in
food may be carcinogenic risks to humans; for example, the chewing of betel nut
with tobacco causes oral cancer. Drink up Socrates, it’s natural.
3. Humans have not had time to evolve a "toxic harmony" with all
of their dietary plants. The human diet has changed markedly in the last few thousand
years. Indeed, very few of the plants that humans eat today, e.g., coffee, cocoa,
tea, potatoes, tomatoes, corn, avocados, mangoes, olives and kiwi fruit, would
have been present in a hunter-gatherer's diet. Natural selection works far too
slowly for humans to have evolved specific resistance to the food toxins in these
newly introduced plants.
4. DDT is often viewed as the typically dangerous synthetic pesticide because
it concentrates in adipose tissues and persists for years. DDT, the first synthetic
pesticide, eradicated malaria from many parts of the world, including the U.S.
It was effective against many vectors of disease such as mosquitoes, tsetse flies,
lice, ticks and fleas. DDT was also lethal to many crop pests, and significantly
increased the supply and lowered the cost of food, making fresh, nutritious foods
more accessible to poor people. DDT was also of low toxicity to humans. A 1970
National Academy of Sciences report concluded: "In little more than two decades
DDT has prevented 500 million deaths due to malaria, that would otherwise have
been inevitable [41]." There is no convincing epidemiological evidence, nor
is there much toxicological plausibility, that the levels of DDT normally found
in the environment or in human tissues are likely to be a significant contributor
to cancer. DDT was unusual with respect to bioconcentration, and because of its
chlorine substituents it takes longer to degrade in nature than most chemicals;
however, these are properties of relatively few synthetic chemicals. In addition,
many thousands of chlorinated chemicals are produced in nature [42]. Natural pesticides
also can bioconcentrate if they are fat soluble. Potatoes, for example, contain
solanine and chaconine, which are fat-soluble, neurotoxic, natural pesticides
that can be detected in the blood of all potato eaters. High levels of these potato
neurotoxins have been shown to cause birth defects in rodents [32], though they
have not been tested for carcinogenicity.
5. Since no plot of land is immune to attack by insects, plants need chemical
defenses – either natural or synthetic – to survive pest attack. Thus,
there is a trade-off between naturally-occurring pesticides and synthetic pesticides.
One consequence of disproportionate concern about synthetic pesticide residues
is that some plant breeders develop plants to be more insect-resistant by making
them higher in natural pesticides. A recent case illustrates the potential hazards
of this approach to pest control: When a major grower introduced a new variety
of highly insect-resistant celery into commerce, people who handled the celery
developed rashes when they were subsequently exposed to sunlight. Some detective
work found that the pest-resistant celery contained 6,200 parts per billion (ppb)
of carcinogenic (and mutagenic) psoralens instead of the 800 ppb present in common
celery [32].
Article reprinted from Mutation Research Frontiers, 7 September 1999
Source: http://ec.europa.eu/environment/archives/ppps/pdf/ma_reding_annex2.pdf
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