Chemicals In Food

Despite recent claims that "natural" foods are safer, there is evidence that "natural" pesticides can be present at much higher concentrations than residues from synthetic pesticides. These "natural" chemicals are often untested and of unknown toxicity, with little evidence of health benefits.

W: are often told that our food is full of poisonous and cancer-inducing chemicals. This is absolutely true! But it is not because of the use of agricultural chemicals. Most food plants contain natural pesticides that, in high-dose tests, are as toxic as synthetic chemicals.

These natural pesticides, such as the flavours of mustard and cabbage, are often the very flavours that contribute to our enjoyment of a plant. The natural pesticides are designed to be toxic, not to titillate our taste buds. Synthetic agrochemicals typically leave residues that are measured in parts per billion, or even parts per trillion. Chemicals made by plants, in contrast, have no Pesticides Board clearance, no maximum dose, no minimum waiting period. The concept that "natural" automatically means "good" because Nature is always

March 1991 Number 19 benign, is a charming legend on a par with Santa Claus and the Tooth Fairy.

Farm-applied synthetic agrochemicals are few in number, and have survived costly and extensive tests for toxicity, teratogenicity (birth defects), and carcinogenicity (cancer-causing).

Natural foods, on the other hand, contain an incredibly complex mix of exotic chemicals. Surprisingly few of these chemicals have been thoroughly tested for safety. There are dozens of flavour constituents in a sprig of parsley (Straten and Maarse, 1983). Some of the parsley flavour chemicals are also found as ingredients in commercial paint strippers. Does this mean that parsley is dangerous? Of course not.

Natural Poisons

Most natural toxins are present at low concentrations. A few can occur at dangerous levels, such as light-activated psoralens in celery and parsnip, cyanide-generating compounds in beans and cassava, poisonous glycoalkaloids in potatoes and poisonous cucurbitacins in throwbacks of squash and cucumbers.

One cultivar of celery, selected for "natural insect resistance", caused March 1991 Number 19 blisters in grocery workers, because the natural resistance was accomplished by higher levels (6-25 ppm) of 5-methoxypsoralen, a DNA cross-linker. Even ordinary celery cultivars can cause long-lasting arm and leg blisters in farm workers, particularly after plant stress. Another "natural resistance" problem arose with the release of Lenape potatoes, which had 3 times the normal level of neurotoxic glycoalkaloids, and had to be withdrawn.

It is of extreme concern that many self-appointed protectors of the environment seem totally unaware of the potential health hazards of natural pesticides. Several infant deaths have occurred when pregnant women took daily doses of herb teas, in the belief that anything "natural" must be harmless (Talalaj and Czechowicz, 1989, 1990).

Although honey is widely regarded as a particularly healthy food, Xenophon's troops were killed in ancient Persia by rhododendron toxins in wild honey, and about half the modern reports of natural food poisoning involve honey. Toxic honey was a significant problem in New Zealand until restrictions on beekeepers were imposed.

Bracken fern, a traditional New Zealand food, is notorious throughout the world for killing cattle, and in Japan is associated with human gullet cancer.

There are many other natural chemicals which in high dose tests are toxic, carcinogenic, or teratogenic, but which are present in lower concentrations in fruits and vegetables. Interestingly, canavanine in alfalfa sprouts (can anything be "greener"?) causes lupus-like symptoms in monkeys fed 40% of their diet as sprouts. The concentration of canavanine is 1.5% of the dry weight of alfalfa sprouts, but I don't know of any reports of problems in humans.

Healthy Poisons?

How can the presence of these potential toxins be reconciled with the considerable evidence that diets rich in fruits and vegetables are associated with low cancer rates? Is there a paradox? Are these minute concentrations of toxins really dangerous?

Natural Toxins Known To Have Harmful Effects

Data collated from various sources including Ames (1983); Ames et al (1987, 1987a)

FOOD

TOXIN

COMMENTS

Beer

alcohol

carcinogen, birth defects

Celery

psoralens

DNA-linker, rash, blindness

Herbal tea, Euphorb (spurge)

phorbol esters

nose & throat cancer

Herbal teas

alkaloids

foetal death

Lupine

anagyrine

birth defects

Mold carcinogens

aflatoxin, patulin

liver cancer

Mold carcinogens

ergot

death, abortion, "witchcraft"

Potatoes

solanine, chaconine

neurotoxin

Squash (throwbacks)

cucurbitacins

toxic

There is a popular school of thought that suggests "even a little bit of poison is too much". The most 'charitable thing one can say about this approach is that it is naive. Four hundred years ago, Paracelsus wrote, Everything is poison. There is nothing without poison. Only the dose makes a thing not a poison.

Are natural chemicals inherently safer than synthetic chemicals? The answer is NO. In a study of several hundred chemicals, about half of both artificial and natural chemicals were carcinogenic at high concentrations (Ames and Gold, 1988, 1990). Similarly when 2,800 chemicals were tested for effects on rodent birth defects, about one-third of either natural or synthetic chemicals tested positive (Ames and Gold, 1990).

Since our diet includes vast numbers of natural chemicals at concentrations that are 1,000 times to 1 million times higher than synthetic chemicals, why is so much emphasis on the so-called risks from synthetic chemicals? Indeed, why so much emphasis on food risks at all?

Perhaps the illogic goes: Bad foods can make us sick, so good foods must be able to make us well. Surveys have shown that the public wants to accumulate enough "health points" by eating "good" foods to overcome other self-destructive actions. Will New Zealand follow the American pattern of becoming a nation of nutritional neurotics?

Are humans somehow able to handle natural toxins better than synthetic chemicals? This is doubtful. In many cases, the body has only general-purpose mechanisms for getting rid of foreign chemicals of whatever origin. What evolutionary device would have prepared humans for the alkaloids of potato and tomato or the chemicals of red pepper — all unknown to the European world until after 1492?

Concentrated Testing

Opponents of synthetic agrochemicals speak obscurely of hypothetical "synergistic" interactions between minute traces of synthetics. But known synergisms don't work that way. Why not worry about the possible interactions between the 4,000-5,000 natural pesticides that we eat in combinations unknown to our ancestors. For instance, I often eat a combination of psoralens, glycoalkaloids, and canavanine — that is, I eat potato salad containing celery and alfalfa sprouts.

How can we interpret the results of toxicity tests performed at high concentrations, compared with actual exposures at very much lower concentrations? Of necessity, compounds are tested at high concentrations where toxic, carcinogenic or teratogenic effects can be measured. This gives an indication of deleterious effects that could be hazardous to workers at industrial dose rates.

After high-dose testing is finished, risks from low doses are calculated by rather dubious means. Using models such as "logprobit", it can be estimated that a very low dosage will cause, say, "one-millionth of a cancer". This model assumes that there is no threshold, that the toxic actions continue in ever diminishing amounts as the dosage is decreased, and that humans are as susceptible as specially bred mice and rats.

As methods of detection continue to improve, the conservative method of calculation implies that it will never be possible to claim zero-risk, only exceedingly low risks. Risks calculated in this manner are thus the maximum risks conceivable within the statistical uncertainties of the measurements. There are, however, a number of reasons why many toxicologists doubt the validity of extrapolating high-dose tests down into the low-dose world.

Test Errors

At high doses, protective mechanisms such as detoxification and DNA repair can be swamped. Low doses may have entirely less drastic effects. One analogy (Ottoboni, 1984) is that of the sports doctor who wants to test the long-term effects of repeated high jumps on joint injuries. Because he can't get 100,000 people to jump 6 meters every day, he gets 1,000 people to jump off a 60 m cliff ten times a day.

Or consider the established dangers of being adrift in an ocean or a large lake. We could find a mathematical relationship between the size of the lake and the chance of drowning. Would this mean that stepping into a puddle is one-millionth of a drowning?

The no-threshold model may not be Valid. One attempt to test this using the known carcinogen 2-acetylaminofluorene at concentrations expected to cause 1% instead of 50% response took 18 months to plan, then 9 months to breed the 24,000 mice needed. Three years and six million dollars later, it still wasn't clear whether there was a threshold (Ottoboni, 1984). Some of the data implied a protective effect at low concentrations of the carcinogen!

This kind of protection is apparently quite common in toxicology (Hayes, 1975; Ottobani 1984). It differs from comparable claims' of homeopathic medicine, where incredibly dilute solutions are purportedly efficacious.

About half the chemicals that cause cancer at high dosages (such as salt and stomach cancer) act by tissue irritation (Ames and Gold, 1990).. In these cases, there should be no induction of cancer when they are present at non-irritating levels.

Because the mathematics of very low dosages are suspect, risks calculated in this manner are perhaps the maximum risks conceivable, within the statistical uncertainties of the measurements. Animal testing procedures predict a tiny risk for many tested chemicals, whether of natural or synthetic origin. Instead of developing neurotic fears of being poisoned by vanishingly small concentrations of chemicals, we should be grateful that modern methods of analysis, combined with high-dose toxicology studies, confirm how insignificant are the health risks from agrochemical residues.

Life Is Risky

How can we measure or compare risks? Is a tiny dose of a potent poison more dangerous than a large dose of a weak poison?

The question is, how does any particular exposure compare with the dose that causes cancer in, say, 50% of rats or mice, with corrections for body weight. This measurement is called the HERP% (Human Exposure / Rodent Potency) (Ames et al, 1987). The larger the value of a HERP%, the more relative risk. The HERP% is only a relative measure of comparative risks. How can it be translated into real terms?

The highest value of 16% is for sleeping pills, yet studies of people who've taken sleeping pills for many years don't confirm any higher cancer rates. On the other hand, drinking 4 glasses of beer (HERP% about 3% per glass) a day is statistically associated with increased risk of throat cancer, probably because alcohol at high concentrations is an irritant. Alcohol is believed responsible for about 3% of all cancers and a number of birth defects; it's a weak toxin that some people consume in large amounts. The risk from "deadly" PCBs and DDT, in contrast, are ten thousand fold less than from a single glass of beer. "The dose makes the poison."

Ames et al (1987a) calculated that drinking a single glass of beer or wine poses a possible teratogenic (birth defect) hazard about the equivalent of eating a kilogram of dirt contaminated with 1 part per billion (10°) of dioxin (TCDD). Since dioxin in New Zealand sanitary napkins was about 1 part per trillion (10-12), I leave it to you to calculate how many kilograms of Tampax would be needed to match the risk from one glass of wine. Wilson and Crouch (1987) discussed the disproportionate fear of TCDD compared with aflatoxin (found in mouldy foods such as peanuts), which is equally as carcinogenic (to rats at least).

Life is too short to waste time worrying about insignificant risks. Is food a significant risk compared to other hazards? We need quantitative information about risks so that we can minimize or remove important risks. This information is available from Risk Analysis, but I've converted it to a new unit called the Butt.

Cigarettes Vs Sex

Since estimates show a loss of life expectancy of about 10 minutes for every cigarette smoked, we can compare other activities with the risk from one cigarette.

Almost everything has some risk associated with it. For a fertile woman, one act of unprotected love-making has a 6% chance of pregnancy (Eiseman, 1980, pg 31), with about 100 deaths per million pregnancies and perhaps 30 years loss of life in such unfortunate cases. The risk from unprotected sex is therefore about equal to the risk from smoking one cigarette. (This is not an either-or situation.)

Risks from food are primarily related to excessive body weight. For instance, the extra calories from one rich dessert are about 5 Butts. Risks from the saccharin in a diet soft drink are a maximum of 0.015 Butts and, because of the biases already discussed, the real hazard is probably much less. Similar considerations would apply to other foods. A glass of beer (near the top of the HERP% table), would be about 0.01 Butts or 10 milliButts.

Historical (epidemiologic) studies can indicate whether environmental factors have been dangerous. Is there really a cancer epidemic related to our widespread use of chemicals.

That so-called epidemic arises almost entirely from lung cancer and is clearly tobacco-related (British Medical Association, 1987). Other types of cancer (skin, prostate, ovaries, and pancreas) have increased slightly because of lifestyle (suntanning) or merely longer life expectancies. Farmers don't show any historical health problems despite greater exposures to agricultural chemicals.

Risks of individual actions

Data from Titterton (1981) converted to "Butts" where 1 Butt = 10 minutes loss of life expectancy (U.S.) Pregnancy risk calculated from Eiseman (1980) pp 30-31 assuming 100 deaths/million pregnancies

Action

Butts

Cigarette (one)

1

Sex, once, unprotected woman (mortality in pregnancy)

1

Rich dessert (one)

5

Soft drink, non-diet

1.5

Soft drink, diet

0.015

Crossing street

0.04

Coast-to-coast drive, US

100

Coast-to-coast, flying

10

Skipping annual PAP test

600

Agrochemicals

What if a political decision should be made to try to eliminate agrochemical residues in all foods? The cost of enforcement, lower yields and higher production costs would almost certainly lead to higher prices and hence less consumption of fresh vegetables and fruits.

As increased consumption of these foods has been shown to be connected with better health, this response to the anti-chemical lobby would damage rather than improve public health. Yet food hazards would not be significantly alleviated, since whatever minor risks do exist arise from naturally occurring chemicals. There is no evidence that any consumer has been harmed by synthetic agrochemical residues as a result of lawful application.

Individual Risks

How do agricultural chemicals rank in the- list of food hazards? The USDA estimated that the greatest risk from food is microbiological; in New Zealand 1 or 2 people a year die from salmonella poisoning. The next greatest risk is too much food or unbalanced diets, followed by environmental contamination (e.g. nitrate), and only then by agricultural pesticide residues and food additives.

Short-lived insecticides can be a potential hazard to agricultural users, compared to the long-term organochlorine pesticides that they replaced. There is no excuse for inadequate safety measures, excessive quantities, inaccurate placement, or insufficient waiting period. This puts the onus of safe application on those who gain an immediate economic benefit.

Risks from pesticides in food arise from natural chemicals, present in both sprayed and unsprayed food. Development of enhanced "natural resistance" could shift more risk to the consumer, unless that natural resistance is carefully evaluated. Most of these risks are quite trivial.

To quote Bruce Ames again: Eating more fruits and vegetables and less fat may be the best way to lower risks of cancer and heart disease, other than giving up smoking. Vitamins, antioxidants and fibre come from plants and are anticarcinogenic. (Ames and Gold, 1990).

There is a strong market for organically grown and/or "chemical-free" foods, and there is no reason why New Zealand producers should not provide food to meet this demand, just as they produce specially killed meat. New Zealand often sells into markets where food is a luxury, not a necessity. We are market-driven, as are the news media whose persistent emphasis on scare stories is a response to the public demand for harmless terror. We should not let the beliefs of this wealthy and well-fed green market cause us to worry that we are at any extra risk by purchasing ordinary, healthy, disease-free produce. Jay D Mann is a plant biochemist at DSIR Crop Research, Lincoln. The opinions expressed in this review are his own, not necessarily those of his employer. This article has been based on a talk presented at the NZ Institute of Agricultural Sciences 1990.

References

Ames, B. N.; Magfaw, R.; Gold, L. S.. 1987. Ranking possible carcinogenic hazards. Science 236, 271-280.-

Ames, B. N.; Gold, L. S.. 1988. Carcinogenic risk estimation (Technical comments) Science 240, 1045-1047.

Ames, B N 1983. Dietary carcinogens and anticarcinogens. Science 221, 1256-1262.

Ames, B N; Gold, LS; Magaw, R. 1987a. Letters. Science 237, 1400.

Ames, B. N.; Gold, L. S$. 1990. Too many rodent carcinogens: mitogenesis increases mutagenesis. Perspective for Science Jun3 8, 1990, pp 1-9

British Medical Association, 1987. Living With Risk (John Wiley, Chichester). Pp 5, 37-39, 117-118.

Eiseman, B. What are my chances? W B Saunders Co, Philadelphia, 1980.

Fieschi, M; Codignola, A; Luppi-Mosca, A. M. 1989. Mutagenic flavonol aglycones in infusions and in fresh and pickled vegetables. J Food Sci 54, 1492-1495.

Hayes, W. J. Toxicology of Pesticides. Williams and Wilkins, Baltimore, 1975.

Lave, L B. 1987. Health and safety risk analyses: information for better decisions. Science 236, 291-295,

Ottoboni, M. Alice. The Dose Makes the Poison. Vincente Books, Berkeley, 1984.

Straten, S.van; Maarse, H. (Eds.). Volatile compounds in food: qualitative data. Division for nutrition and food research TNO, AJZeist, The Netherlands, 1983.

Talalaj, S.; Czechowicz, A. Herbal remedies — harmful and beneficial effects. Hill of Content, Melbourne, 1989.

Talalaj, S.; Czechowicz, A. 1990. Cautions for use of herbal remedies during pregnancy and for small children. Medical Journal of Australia, in press.

Titterton, E. 1981. Risk, safety, costs and common sense. Interdisciplinary Science Reviews 6, 333-339.

Wilson, R., Crouch, E. A.C. 1987. Risk assessment and comparisons: an introduction. Science 236, 267-270.

Young, A. L. and Reggiani, G. M. (Ed.) Agent Orange and its associated dioxin: assessment of a controversy. Elsevier (NY) 1988.