Corn toxin examined in border birth defects
Diet may have put Hispanics at risk
By Laura Beil / The Dallas Morning News
[Mod: Please visit the website for this article, which looks at every
useful aspect, including dose, mechanism, time variability and
interactive risks - G)
The nurses at Valley Regional Medical Center in Brownsville sensed
something more than a horrible coincidence. Two babies born the same day
in April 1991 had brains that were stunted or missing, a rare defect
that usually strikes only three or four births in 10,000.
State and national investigators would eventually find that Brownsville
had an astonishingly high rate of anencephaly, as the condition is
called. From 1989 through 1991, 32 women in this town of 130,000 carried
anencephalic babies. Many of the children died within hours, and all
within days, of birth.
Then, in 1992, the anencephaly rate ebbed as unexpectedly as it had
Still searching for a cause, many experts keep circling back to one of
the few explanations for an epidemic that can come and go on its own: a
natural poison that crept in and out of the food supply. Disease
investigators have focused on a common toxin found in corn, a mainstay
of a traditional Mexican-American diet. If this toxin is indeed
responsible for the birth defects that stalked the Lower Rio Grande
Valley and no one has yet concluded that it is then Texas health
officials worry about other effects in Hispanics. In addition to birth
defects, the chemical may increase the risk for esophageal and liver
The outbreak of 1991 remains unsolved. From the beginning, many
residents suspected the pesticides that armor nearby fields of cotton
and sorghum. Others blamed the chemicals that waft from industries along
the Rio Grande. Some parents of affected infants even shared a $17
million settlement from more than 80 maquiladoras U.S. factories
hugging the Mexican side of the river in 1995.
But now, state health officials wonder whether the culprit was not
man-made, but a natural fungus that can cling to corn. The fungus makes
a toxin, called fumonisin, unknown to science until 1988.
Given fumonisin's potential to cause disease, a United Nations committee
will soon release its first report recommending a daily limit on human
exposure to the toxin. Last summer, the U.S. Food and Drug
Administration announced possible guidelines for the maximum amount of
fumonisin in corn intended for human food. The agency recommends no more
than 4 parts per million for masa and similar corn products.
But the FDA number, state officials argued in a three-page response, may
be too high for those who depend on corn for their daily bread. "There
is clear evidence," state officials warned, "that fumonisins are
carcinogenic in some animal species and sufficient evidence indicating
that these compounds may be able to affect the neural development of the
Fumonisin (pronounced few-MAHN-i-sin) is spit out by the mold Fusarium
as part of its chemical defense system. For decades, farmers and
ranchers have known that animals can fall seriously ill if they eat corn
that has been coated with Fusarium, even if the kernels later seem
clean. People in parts of the world with high Fusarium growth, most
notably the Transkei region of South Africa, have high rates of
But it wasn't until 1988, when South African scientists first described
fumonisin, that anyone knew exactly why the mold was dangerous.
One of the more peculiar traits of fumonisin is its ability to cause
vastly different diseases in different animal species. Pigs that eat
fumonisin-contaminated corn can develop pulmonary edema, a condition in
which their lungs fill with fluid. The most sensitive animals appear to
be horses, which get a crippling brain disease called
In humans, hints of the esophageal and liver cancer risks come from
studies in rats, and from parts of the world such as the Transkei and
certain areas of China with frequent fumonisin contamination of corn.
Health officials note that these regions also have high rates of the
same birth defects that appeared in the Rio Grande Valley. But this kind
of research doesn't address the possibility of a coincidence.
Possible fetal effects
Anencephaly, which befell Brownsville's babies, is one of a cluster of
abnormalities called neural tube defects. The most common is spina
bifida. The defects occur soon after conception, at a time when a woman
wouldn't even know she is pregnant. They happen when the cells of the
embryo that will create the central nervous system don't wrap around
themselves and form a tube during development. Sufficient levels of
folic acid, a B vitamin, will protect against neural tube defects.
In 1997, researcher Victoria Stevens of Emory University in Atlanta
offered a possible connection between fumonisin and folic acid. In
test-tube experiments, she found that fumonisin interfered with a cell's
ability to absorb the vitamin. If this is true in the womb, then
fumonisin might starve a developing embryo of its protection.
much more at website
Gary N. Greenberg, MD MPH Sysop / Moderator Occ-Env-Med-L MailList
gary.greenberg at duke.edu Duke Occupat, Environ, Int & Fam Medicine
OEM-L Maillist Website: http://occhealthnews.com