The federal government is considering new limits in food on a naturally occurring, highly carcinogenic toxin found in many common grains and linked to deaths of hundreds of young people in Third World.

Food industry leaders claim the action may force them to remove all jars of peanut butter from grocery shelves and halt or limit the interstate commerce of other grains, including corn.

The first traces of what is now called aflatoxin, produced by a common mold, were identified a quarter century ago in Britain in a batch of fungus growing on imported peanut meal. The meal was consumed by flocks of ducks and turkeys being fattened for Christmas. They all died.

“There’s no doubt humans have been exposed to (the toxin) over the eons of time, since the beginnings of agriculture,” said Paul Newberne, a pathologist at the Massachusetts Institute of Technology who conducted many of the early experiments on the compound. “But science has only recently learned of it, and it’s taken time to react on that knowledge.”

Larger doses of aflatoxin are highly poisonous to humans as well. In 1975, 106 children and young adults in western India died of chronic hepatitis brought on by eating locally grown corn infected with aflatoxin. The poison was nurtured by a wet harvest and poor storage conditions. In Mozambique three years ago, scientists found a direct correlation between an epidemic of liver cancer a relatively rare disease and the common local diet of aflatoxin tainted milk and grain.

There has never been a clinically proven case of aflatoxin poisoning in the United States, but the substance is believed to be a crucial, if disguised, component in the development of chronic diseases. Even in miniscule body’s ability to fend off chronic disease. It has been linked to cancer of the liver, stomach, the digestive system and throat. “In the western world, they are responsible for promoting a wide range of chronic disease,” said Peter Austrick, an English microbiologist and aflatoxtin expert, “It appears to function in much the same way that AIDS (acquired immune deficiency syndrome) does, destroying the body’s defenses.

“Aflatoxin may be the missing link in explaining a lot of mysteries,” he said. “After all, nobody knows what causes 80 percent of the cancers of the world.” One form of cancer he believes needs to be investigated for aflatoxin influence is breast cancer.

“Breast cancer is distributed in the cold areas like Sweden, Sies, ’aid Austrick. “There are certain types of fungus which grow only in these same areas because of the climate. There’s evidence that there is a connection, but little research has been conducted.”

Said William Lijinsky, a Maryland researcher associated with the early English experiments: “(Longterm aflatoxin consumption) may be the story behind Reagan’s (colon) cancer.”

The problem with new regulations now being mulled over by the Food and Drug Administration is the fact that aflatoxin producing mold is ever-present in nature, and impossible to completed in roughly 50 different foods ranging from millet to Brazil nuts to

Cottonseed to corn. Its odor is easily recognized it accounts for the heavy, pungent smell of new mown hay. Cooking and processing do not destroy the toxin it produces.

 

“The (aspergillus) spores are floating around in the air all the time,” said Lijinsky. “You can’t find a place where the fungi don’t occur.”

Yet aflatoxin is the “most potent carcinogen known in laboratory animals,” according to the National Academy of Sciences, and there is no known safe level for hold.

Lijinsky, now working in association with the National Cancer Institute, used extracts of the toxin so small the total fed each laboratory animal could be contained on the head of a pin. His rat colony died within 18 months. MIT’s Newberne broke the substance down to its smallest unit possible using modern equipment one part per billion and fed it to cancer sensitive rats. His 300 rats all developed tumors.

“Technically I got as low as you could get,” said Newberne.

Article extracted from this publication >>  August 2, 1985