Pesticides in Milk
The Environmental Protection Agency (EPA) allows up to 60 times more
pesticides in feed given to cows than in crops grown for human consumption.
Unless you eat organic fruits and vegetables, for every portion of broccoli
or rice or corn you eat, you'll ingest one dose of various pesticides. Should
you eat corn every day for two years, you'll absorb 730 doses. Corn
grown for cows might contain 60 times the amount of pesticide. Cows eating
corn every day for two years might then ingest 43,800 doses. A human sitting
atop the food chain drinking one glass of milk or eating one portion of
tainted muscle from her leg or back will absorb concentrated pesticides. Eat
her face (at Burger King) or her hind (at Wendy's) and you might ingest more
than 15 million doses of pesticides each year. That adds up to over 1 billion
doses during your lifetime.
The scientific facts:
http://www.notmilk.com/pesticides.html
Robert Cohen
http://www.notmilk.com
U.S. government scientists from the Centers for Disease
Control have released a new study revealing that switching to organic foods
provides children with "dramatic and immediate" protection from toxic
pesticides. The scientists tested the urine of elementary school children for 15
days. Children ate conventional foods for ten of the days and ate organic foods
for five days. During those five days, researchers saw the toxins malathion and
chlorpyrifos in the children's urine completely disappear. These chemicals are
two of the most commonly found pesticides on non-organic foods, and are
associated with nerve damage in children. Pesticide levels increased five-fold
in the children's urine as soon as conventional foods were reintroduced to their
diet. The study concludes, "An organic diet provides a dramatic and immediate
protective effect against exposure to organophosphorus pesticides that are
commonly used in agricultural production."
http://www.organicconsumers.org/school/organicstudy090405.cfm
Another reason to go organic.....
http://www.commondreams.org/archive/2007/05/27/1487/
Published on Sunday, May 27, 2007 by the Los Angeles Times
Plantation Workers Look for Justice in the North
by T. Christian Miller
CHINANDEGA, Nicaragua - The people crammed into the stifling basketball gym.
They filled the court, lined the walls and tumbled beyond the doors onto the
sun-blistered streets.
They had gathered to hear a promise of justice.
Many had spent their lives toiling on banana plantations that U.S. companies
operated in this region some 30 years ago. By day, the workers had harvested
bunches of fruit to ship to North American tables. At night, some had sprayed
pesticide into the warm, humid air to protect the trees from insects and rot.
As the decades passed, the workers came to believe that the pesticide, called
DBCP, had cost them their health. Prodded by U.S. lawyers, thousands joined
lawsuits in the U.S. and Nicaragua alleging that the pesticide made them
sterile.
The U.S. firms that sold and used the pesticide have never faced a U.S. jury
trial over its use abroad. Last month, a Los Angeles attorney named Juan J.
Dominguez stood before a sea of nearly 800 dark, hard faces and predicted that
the day of reckoning was at hand.
“We are fighting multinational corporations. They are giants. And they are going
to fall!” Dominguez thundered.
The crowd exploded. They leapt to their feet, waved their hats, shook fists in
the air. “Viva! Viva!” they chanted.
The scene last month foreshadowed a legal drama set to play out in a Los Angeles
courtroom this summer, when a lawsuit filed by Dominguez and his partners could
end a struggle that has sprawled across three decades and courtrooms on four
continents.
For the first time, a U.S. jury will have the chance to weigh the accusation
that Dole Food Co. knowingly used a pesticide manufactured by Dow Chemical Co.
that sterilized workers in Latin America three decades ago.
The complexity, history and geographic spread of the case demonstrate how legal
systems have failed to keep pace with the rapid movement of goods across
international borders. Jurisdictional and procedural issues have repeatedly
impeded attempts to sue U.S. companies in the United States for alleged
wrongdoing in other countries.
“The question is where do we litigate these issues,” said Alejandro Garro, a
Columbia University law professor and expert in international law. “The answer
is that we don’t have a global law. We are building it on a case-by-case basis.”
Dole, the Westlake Village-based food giant, and Dow, of Midland, Mich., deny
the allegations. Both companies acknowledge that the pesticide DBCP has been
linked to sterility in men exposed to it while manufacturing it in factories.
And both companies acknowledge that the product was used in Nicaragua’s banana
fields.
But the companies contend that there is no proof that DBCP (dibromochloropropane)
sterilized any field worker. The quantities of DBCP used were too small, and the
open-air conditions too diffuse, to cause harm, the companies say.
“Dow views most of today’s claims relative to the product as without merit,”
said Dow spokesman William Ghant. Dow acknowledged that the possibility of harm
existed but said the product was safe as long as instructions were followed.
Dole said it applied DBCP in Nicaragua 13 times in the 1970s, with each spraying
lasting about two weeks. The pesticide was an effective killer of tiny worms
that caused the roots of banana plants to rot.
“There is no reliable scientific evidence at all that points to this pesticide
causing any injury to field workers in the open air environment,” said Michael
Carter, Dole’s general counsel. “There is no science to support that. None.”
Earlier this month, Los Angeles County Superior Court Judge Victoria Chaney made
a ruling that broadened the potential reach of the case.
Chaney linked Dominguez’s case with four other pending lawsuits in Los Angeles
involving sterility claims on behalf of more than 3,000 former banana workers
from Costa Rica, Honduras, Guatemala and Panama. In addition to Dow and Dole,
Del Monte Fresh Produce Inc., Chiquita Brands Inc. and Shell Oil Co. are named
as defendants in those cases.
Cincinnati-based Chiquita declined comment on the lawsuit but said it used the
chemical briefly in the 1970s in Panama and Costa Rica. Shell said it sold no
DBCP in Central America after 1974 and that “few, if any” banana workers were
harmed by its product. Del Monte said it used the pesticide briefly in Costa
Rica and Guatemala and declined further comment.
In the middle of the dispute are this region’s people. The case has spread its
own kind of toxin, infecting every facet of life in this fertile bottomland
wedged between volcanoes and the ocean on Nicaragua’s Pacific Coast.
After 30 years of being told they have been poisoned, locals tend to blame the
region’s many health and environmental woes on DBCP.
They call themselves the afectados - the affected ones.
13 men, 1 lawsuit
Jose Adolfo Tellez never wanted to be a legal pioneer.
With dark hair and a broad, round face, Tellez lives in a two-room cinder-block
house in Chichigalpa, a town in the heart of Nicaragua’s banana zone.
Early each morning he rides his battered black mountain bike seven blocks along
rutted streets to the central market, a chaotic warren of shops where beef hangs
in strips and baskets of papaya are lighted by shafts of sunlight.
Tellez haggles over prices before the day’s damp heat descends. Heading home, he
spends a cordoba - about 5 cents - for a brick-sized block of ice to chill his
meat and vegetables.
His main job is tending to his mother, 80, who shuffles across the home’s
concrete floors with a donated walker. There is no one else to do the job.
Tellez, 58, has no children, no wife, to help him.
He blames DBCP.
Tellez is the lead plaintiff in Tellez vs. Dole, scheduled for trial July 2. He
joins a dozen other named plaintiffs, all of whom have had tests administered by
their lawyers showing that their semen does not contain sperm.
Tellez believes that he became sterile after going to work outside the small
town of Posoltega, 15 miles southeast of here, where Dole began operations in
Nicaragua in the late 1960s.
On the plantation, where long, green alleys of banana trees stretched across
more than 1,400 acres, he harvested bananas, cut weeds from the plants, trimmed
leaves and hauled irrigation tubes.
Tellez said he was never given protective gear while working in the fields. Nor,
he said, did anyone tell him that DBCP could cause sterility.
“They told us to go to work, and we would go to work,” Tellez said.
Tellez married, but he and his wife were unable to have children. She eventually
left him to live with another man, Tellez said, and soon had a child.
Tellez had thought his wife had the problem. But tests showed he was sterile.
In the macho culture of rural Nicaragua, children are a measure of wealth and
power. Tellez had neither. He was labeled a buey - slang for a castrated bull.
“It demoralized me,” he said. “I felt like a useless man.”
Sterility and pesticide
Epidemiological studies have confirmed that DBCP causes sterility in human
males, according to the U.S. Agency for Toxic Substances and Disease Registry.
Evidence of other human health effects is less clear. However, lab animals
exposed to DBCP have developed stomach and lung cancers and kidney and brain
damage, according to the agency.
DBCP’s toxicity first made news in 1977, when about three dozen factory workers
at an Occidental Petroleum Corp. subsidiary in Lathrop, Calif., where pesticides
were mixed, reported problems having children. Tests showed the factory workers
had zero or below-normal sperm counts.
Within months, the EPA had suspended most uses of DBCP. Government hearings
revealed that Dow and Shell Chemical Co., then a subsidiary of Shell Oil Co.,
the primary makers of DBCP, had long known about its dangers. Tests dating to
the 1950s showed the chemical atrophied lab animals’ testes.
Workers began filing lawsuits. In 1983, Duane Miller, a young Sacramento
attorney, won a $4.9-million judgment against Dow on behalf of six Occidental
workers. Two years later, the EPA permanently banned the use of DBCP in the
United States.
It was the first skirmish in a legal war that soon spanned the globe.
U.S. law firms began suing in U.S. courts on behalf of workers in other
countries - more than 50,000 plantation workers over 30 years in countries
including the Philippines, Nicaragua, Costa Rica and Ivory Coast. The defendants
have been the manufacturers of DBCP - Dow and Shell - and the fruit companies
that used it: Dole, Del Monte and Chiquita.
Nearly every case ran into the legal doctrine forum non conveniens, which says
lawsuits should be heard in the countries where the damage occurred. Lawyers for
the companies convinced judges to transfer the cases to the countries of origin.
In practice, that stalled the lawsuits for years. Complex trials bogged down in
ill-equipped Third World courts. Plaintiffs’ law firms lacked money to pursue
cases in foreign countries.
The companies settled some cases without admitting culpability. In 1992, several
firms reached a settlement in which $20 million was paid to 1,000 Costa Ricans.
In 1997, Dow and other companies paid $41.5 million to 26,000 workers worldwide.
The money was divided among thousands of plaintiffs. After attorneys’ fees, some
workers received no more than a few hundred dollars.
By the late 1990s, banana workers and attorneys were frustrated by their
inability to get a case before a U.S. jury, with the potential for higher awards
and, more important for some, a finding of wrongdoing by the companies.
New rules in court
Then Nicaragua changed the rules. In 2000, its legislators passed a special law
to facilitate DBCP lawsuits.
The law stacked the deck in favor of the workers: DBCP was automatically
considered the cause of sterility in any banana worker. Companies had to deposit
$100,000 with Nicaraguan courts simply for the opportunity to defend themselves.
In December 2002, a Nicaraguan judge awarded nearly $490 million to about 450
workers. Other big judgments followed. Dow and Dole have so far blocked attempts
to enforce the Nicaraguan judgments in U.S. courts.
The new law made Nicaragua hostile territory for Dow, Dole and other defendants.
That created an opportunity for new lawsuits in the United States, which Dole
and Dow no longer opposed.
Dominguez, perhaps best known for his ubiquitous personal-injury ads on Los
Angeles buses, seized the opportunity. He partnered with Sacramento attorney
Miller, who had filed the first DBCP lawsuits in the U.S. nearly 30 years
earlier, and they filed suit in Los Angeles in 2004.
To build the case, Dominguez opened an office here, in the center of Nicaragua’s
banana belt. He connected with local union bosses, ran advertisements on the
radio, even sponsored a local baseball team.
Thousands came forward to provide sperm samples in a back room set up in
Dominguez’s office, a yellow and brown one-story building near the main square
here. The samples were analyzed by a laboratory paid for by the attorneys.
Dominguez and Miller filed legal briefs citing old corporate documents which,
they said, showed that Dole officials were aware of the dangers. In a 1978 memo,
a top Dole official warned that implementing all the procedures in a guide for
safe use of DBCP was “well nigh impossible.”
“Did they warn you about this? No,” Dominguez told another crowd at a recent
rally. “Did they put you in danger? Yes.”
Although only 13 plaintiffs have been named in the U.S. suit, a victory could
result in settlements for the thousands of other former banana workers who can
show sterility problems. An original defendant in the Tellez case, Amvac
Chemical Corp. of Newport Beach, settled for $300,000 last month.
Dominguez has registered about 12,000 clients in Nicaragua alone. Worldwide, the
number of possible clients is estimated to be hundreds of thousands.
Dole and Dow have long experience with such lawsuits. In some instances, the
companies have been able to show that supposedly infertile men fathered
children. The companies have also discovered plaintiffs who did not work on
farms that used DBCP.
Dole has settled some cases directly with workers. It recently announced a
program in Honduras to pay up to $5,800 to banana workers who agreed to drop
their claims against the company. The company is seeking a similar accord in
Nicaragua. Such settlements, Dole said, were not admissions of wrongdoing.
“We don’t want to spend our lives forever dealing with this, so the company has
adopted an approach to find a reasonable resolution to these pending claims,”
said Carter, Dole’s general counsel.
History of contamination
It is not easy to show that DBCP caused a worker’s sterility or health problems,
especially in a poor country like Nicaragua.
The region around Chinandega has long been dominated by agriculture, producing
cotton, sugar cane and other crops. For decades, growers - from both the United
States and Nicaragua - sprayed DDT, DBCP and other highly toxic pesticides, many
linked to developmental or health problems.
Seven studies conducted from 1995 to 2002 found contamination in community
wells. Locals routinely drink water tainted with pesticides, said Valeria
Delgado, an investigator at Nicaragua’s Center for the Investigation of Water.
None of the studies tested specifically for DBCP.
Studies have also found that water supplies are laced with fecal matter and
other pollutants. Medical care is scarce. Diet is subsistence level. Many of the
men drink heavily.
Medical officials acknowledge that they have no proof, just strong suspicions,
that the town’s ills are linked to pesticides.
“If you work in this environment and you wind up sick, I can presume it’s an
effect of chemical intoxication,” said Yolanda Garcia, a toxicologist at the
local clinic. “I can presume, but I can’t prove.”
Death of a mother
All across Nicaragua’s banana region, in churches and classrooms, at funerals
and bars, DBCP is blamed for every illness.
One hot day last August, Leticia Vidabre, 63, lay dying on a mattress on the
concrete patio behind her house.
A neighbor waved a folded piece of paper to keep off the flies. Acrid smoke
wafted from a nearby cooking fire. Next door, salsa music blared.
Slipping in and out of consciousness, Vidabre struggled to tell her story. She
worked in the packing section at one of Dole’s plantations, she said, putting
bananas into boxes for shipping to the United States.
She said she believed that washing the bananas and drinking water on the
plantations had exposed her to DBCP. After 16 years of working on a plantation
called San Pablo, Vidabre began to feel sick. Her back hurt. Headaches were
constant. She quit and became a housewife.
“When I started work at San Pablo, I was healthy. When I left, I was in a bad
way,” she said.
Last year, a doctor told her that her kidneys were not functioning well. A large
woman with heavy lips and eyes, Vidabre began spending her days in bed.
“Those bananas weren’t for us,” she said. “But so many of us have died.”
A month later, on Sept. 6, Vidabre died. She was buried in the town cemetery,
just down the road from the old banana plantation.
Her relatives blamed the pesticide. But nobody really knew.
t.christian.miller@latimes.com
Copyright 2007 Los Angeles Times
Not just hitchhikers: human pathogens make homes on plants
Susan Milius
http://findarticles.com/p/articles/mi_m1200/is_16_172/ai_n21079946
Jeri Barak's tomato plants have a weird disease breaking out on them. Not the
biggest surprise, perhaps, since she's a bona fide U.S. Department of
Agriculture plant pathologist. But what's afflicting Barak's tomatoes isn't some
everyday farm ailment--their leaves are colonized with Salmonella enterica, more
famous as an animal pathogen. This bacterium leads to about 600 deaths in people
each year, along with 40,000 reported eases of illness.
It's the species that everyone's supposed to guard against when handling raw
meat, eating undercooked eggs, or petting baby turtles. Barak, however, has
started studying this animal pathogen's role on plants. And she's not talking
about bacteria just passively smearing plants like streaks of dirt.
]
Evidence has been growing that high-profile human pathogens, such as salmonella
strains and the deadly Eseherichia coli O157:H7, actively colonize plants. In
doing so, the pathogens follow variations on their attack tactics for animals.
They grow structures to glue themselves in place. They build defensive shields
and fortresses. They set up housekeeping. Barak doesn't go so far as to say that
salmonella and E. coli make plants sick, but these human pathogens are
definitely up to something on plants.
Understanding what human-disease organisms do when they go plautside could
suggest new ways to combat foodborne illnesses, says Barak. Produce is
increasingly often the culprit behind disease outbreaks, and cases such as the 3
people killed and more than 200 sickened in 2006 from eating tainted fresh
spinach have dramatized that food safety begins with the food, not its handlers.
The people-plant-pathogen interplay inspired a special symposium at last July's
annual meeting of the American Phytopathological Society in San Diego. Some
pathogen species literally do cause diseases in both plants and people (see
sidebar). Other microbes typically don't hurt plants as much as they hurt
people. Still, plant pathologists say that discovering how these microbes set up
housekeeping on plants could lead to new ways to stop them. Barak, of the USDA
in Albany, Calif., told her colleagues at the meeting that although plant
pathologists had for decades deferred to human-disease specialists in the study
of these pathogens, "now we need to take back salmonella."
PLANT LIFE Just what salmonella and E. coli are up to on plants didn't get much
attention until recently. "It wasn't until people started getting sick from
fresh produce that [we] started looking at how pathogens do this;' says
Barak.According to statistics from the Centers for Disease Control and
Prevention (CDC) in Atlanta, only 0.6 percent of disease outbreaks from food in
the 1970s could be traced to fresh produce. In the 199Os, however, produce
accounted for 12 percent of outbreaks, and since a 1998 revision of surveillance
criteria, the percentage has edged up to 14.
Many factors have contributed to the rise in killer fruits and vegetables.
People today eat almost a third more fresh produce than they did in the 1970s.
And today's produce comes from an international and industrialized system in
which it often travels farther than the people who eat it. Outbreak-tracing
techniques have improved too.
The increase in outbreaks inspired new research on produce safety and led to
disturbing findings. Even a few years ago, Barak says, microbiologists had
assumed that human pathogens were merely passengers on plants, and so could be
dealt with by soap and water. But in test after test early in this decade, none
of the available washes and sanitizers could clean produce completely. The
persistence of bacteria prompted researchers to wonder whether pathogens were
making more than merely casual contacts with plants.
Tests showed that pathogens, either passively or actively, could infiltrate
tissues far beyond the reach of surface washes. For example, Red Delicious
apples dunked in water containing E. coli O157:H7 in a lab test ended up with
the bacteria inside the core even though the fruit hadn't been cut. The bacteria
in this experiment carried a gene that made them fluoresce green, and the glow
showed the bacteria near the seeds, Larry Beuchat of the University of Georgia
in Griffin and his colleagues reported in 2000.
Other experiments have shown E. coli seeping into uncut, unpeeled oranges
through the little break in the skin where the fruit parts from its stem. Mangos
and tomatoes likewise are vulnerable to salmonella through their stem scars.Even
pathogens that didn't lurk deep in tissues proved virtually indelible. By 2002,
at least four studies had confirmed that neither chlorine treatment nor a good,
brisk scrubbing dislodged E. coli from lettuce. Current research is addressing
this challenge (SN: 12/16/06, p. 394), but the failure of most washing systems
has clued researchers in to a secret of E. coli contamination: The bacterium
gets a grip on plants and hangs on.
Studies of other pathogens similarly came to the conclusion that pathogens
actively colonize plants. Maria Brandl, also of USDA's Albany lab, followed up
on a 1999 salmonellosis outbreak in California by testing a bacterial strain of
S. enterica called serovar Thompson, which had been isolated from a patient.
After inoculating chopped eilantro leaves and even some salsa with the strain,
Brandl reported that the bacterium grew quickly to high concentrations in both
foods.
Brandl and her USDA colleague Robert Mandrell then took their test to live
plants. They inoculated growing eilantro leaves with a pathogenic salmonella
strain as well as with two bacterial species common on plants. All three
microbes grew and colonized the leaves. The salmonella strain didn't flourish as
abundantly as the specialized plant bacteria, but it did establish a presence on
the leaf.
When the researchers stressed the bacteria by keeping the leaves dry, the
salmonella population shrank but rebounded when Brandl rehumidified the plants.
The salmonella strain responsible for the 1999 poisonings was a perfectly
plausible leaf colonizer, Brandl and Mandrell reported in 2002.
Ordinary diseases of the plants, which are otherwise harmless to people, may
help the human pathogens make themselves at home. Growing in a test tube, E.
coli O157:H7 doesn't reliably make a protective biofilm. But when researchers
added the E. coli to test tubes along with a regular plant bacterial pest,
Erwinia chrysanthemi, the human pathogens readily joined the biofilm of the
plant pathogen.
Barak is now working on a study with whole plants. She and her colleagues are
finding that salmonella grows more abundantly if a plant is already infected by
Xanthomonas campestris pathovar vesicatotoria, which causes bacterial spot
disease on peppers and tomatoes.SURVIVOR To tease out the genetic mechanisms
behind salmonella's ability to make itself at home on a plant, Barak and her
colleagaues worked their way through a set of experimentally created mutants of
a strain called serovar Newport. The researchers found mutants that couldn't
attach themselves to alfalfa sprouts, a common source of disease outbreaks.
Analyzing the genetic defects in these bacteria gave Barak a clue as to what
genes the bacteria use when confronting a leaf. "It was ironic," says Barak,
that 13 out of 20 of these mutants had disruptions in genes that had never been
characterized in years of previous work on how sahnonella infects animals.
That discovery implies that the bacteria cope with plants by using some of the
same genes that power pathogenic attacks on animals--for example, a gene for
strands of protein nicknamed Taft, which attach the bacterial cell to a surface.
Taft have attracted attention from Alzheimer's researchers trying to understand
how protein deposits build up outside cells in failing brain tissue. But as
Barak's work shows, salmonella cells apparently also have devices specifically
for making solid attachments to plant surfaces. The latest paper from this
project, in the September Molecular Plant-Microbe Interactions, details two such
fasteners. The molecular gadgets help the microbes hold on to each other as well
as to plant tissue. The interconnected bacterial cells form a solid biofilm,
which offers protection to its members from external hazards.
Such capacity for living on a plant doesn't surprise Barak. "I think colonizing
plants may be vital for salmonella to live out their life cycle" she says. Any
such animal pathogen has to survive occasional periods when it's outside the
warm, plush world of an animal host. By comparison, a plant leaf is harsh, with
no temperature regulation or protection from drought, deluge, or ultraviolet
blast. Landing on a plant "is like Salmonella going to the moon," Barak says. So
it makes sense that pathogens maintain equipment for emergency landings on
plants.The hardships of life in a crop field have other effects important to
people, according to Karyn Meltz Steinberg of Emory University in Atlanta.
People who get sick may just be collateral damage in a war between bacteria and
their protozoan predators. She and her Emory colleague Bruce Levin have been
musing about what benefit E. coli, a microbe with hoofed mammals as its natural
host, gets from killing people.
The pathogen's toxin might defend the bacteria against grazing protozoa
typically encountered outside one of those hoofed hosts, such as in soil. Meltz
Steinberg and Levin tested the idea by tracking E. coli's survival with and
without the presence of the rapacious, bacteria-hunting species Tetrahymena
pyriformis. An E. coli strain carrying a toxin-making factor outperformed a
harmless strain only when stalked by the protozoans, the researchers reported in
the Aug. 22 Proceedings of the Royal Society B. Even though life on plants may
be a stretch for human pathogens, they can be very hard to kill there. Abetter
strategy, Barak says, is to improve farming practices so as to limit the spread
of bacteria to crops. To keep food safe, "we've got to give farmers the tools",
she says.
The Albany research program includes efforts to find possible routes of
agricultural contamination. Barak's been studying the life of salmonella in
soil, where other research has suggested that the bacteria can survive at least
for a while. In the lab, she mimicked a farmer discovering a contaminated crop
of tomato plants, plowing them into the soil, waiting a week, and then planting
new seeds. Even 6 weeks after reseeding, she found salmonella on the second
crop.
The way in which water is used on farms could also be a problem, according to
several labs. For example, the USDA lab in California has recovered E. coli
O157:H7 from lettuce seedlings days after experimentally irrigating them with
tainted water. And when the Beuchat group painted a salmonella solution onto
tomato blooms, 2 of the 8 fruits that formed from those flowers carried the
pathogen. Farmers don't go around dabbing their crops with dirty paintbrushes,
but they have felt free to use untreated water from the farm for spraying
pesticide mixes. Barak speculates that someday farmers might have to make sure
they use clean drinking water in their sprayers. These and other routes of
contamination need investigating, she says.
In the meantime, she offers comfort--with some cautions--to fans of fresh fruits
and vegetables. "Flare-ups of food pathogens are rare events;' she says. To
minimize her own chance of encountering worrisome bacteria, she avoids damaged
fruits and vegetables. They leak moist innards of the plant and offer fertile
ground for pathogen picnics. And she minimizes store-to-fridge time as much as
she can. "I tell people: 'Treat your produce like ice cream.'"
Even with her research on the dark side of salad, she hasn't given up. "Oh, I
eat this stuff," she says. "I'm a vegetarian."
COPYRIGHT 2007 Science Service, Inc.
COPYRIGHT 2008 Gale, Cengage Learning
http://www.jacn.org/cgi/content/abstract/12/4/412
Niacin deficiency and cancer in women
E. L. Jacobson
Dept. of Clinical Sciences, Markey Cancer Center, University of Kentucky,
Lexington 40536-0080.
A new interest in the relationship between niacin and cancer has evolved from
the discovery that the principal form of this vitamin, NAD, is consumed as a
substrate in ADP-ribose transfer reactions. Poly(ADP-ribose) polymerase, an
enzyme activated by DNA strand breaks, is the ADP-ribosyltransferase of
greatest interest with regard to effects on the niacin status of cells since its
Km for NAD is high, and its activity can deplete NAD. Studies of the
consequences of DNA damage in cultured mouse and human cells as a function of
niacin status have supported the hypothesis that niacin may be a protective
factor that limits carcinogenic events. To test this hypothesis in humans, we
used a biochemical method based on the observation that as niacin nutriture
decreases, NAD readily declines and NADP remains relatively constant. This has
been demonstrated in both fibroblasts and in whole blood from humans. Thus, we
use "niacin number," (NAD/NAD+NADP) x 100% from whole blood, as a measure of
niacin status. Healthy control subjects showed a mean niacin number of 62.8 +/-
3.0 compared to 64.0 for individuals on a niacin-controlled diet. Analyses of
women in the Malmo Diet and Cancer Study showed a mean niacin number of 60.4
with a range of 44 to 75. The distribution of niacin status in this population
was nongaussian, with an unpredictably large number of individuals having low
values.
(http://www.cancersolutions.org/2008/02/niacin-and-cancer_06.html)
Cancer and Niacin Study,
Studies of cultured cells (in vitro) provide evidence that NAD content
influences the cellular response to DNA damage, an important risk factor in
cancer development. Cellular NAD is consumed in the synthesis of ADP-ribose
polymers, which play a role in DNA repair, and cyclic ADP-ribose may also
mediate cell-signaling pathways important in cancer prevention (11).
Additionally, cellular depletion of NAD has been found to decrease levels of the
tumor suppressor protein, p53, in human breast, skin, and lung cells (10).
Neither the cellular NAD content nor the dietary intake of NAD precursors
(niacin and tryptophan) necessary for optimizing protective responses following
DNA damage has been determined, but both are likely to be higher than that
required for the prevention of pellagra. Niacin deficiency was found to
decrease bone marrow NAD and poly-ADP-ribose levels and increase the risk of
chemically induced leukemia (12). Moreover, one study reported that niacin
supplementation decreased the risk of ultraviolet light-induced skin cancers in
mice (13). However, little is known regarding cellular NAD levels and the
prevention of DNA damage or cancer in humans. One study in two healthy
individuals involved elevating NAD levels in blood lymphocytes by
supplementation with 100 mg/day nicotinic acid/day for eight weeks. Compared to
non-supplemented individuals, the supplemented individuals had reduced DNA
strand breaks in lymphocytes exposed to free radicals in a test tube assay (14).
More recently, nicotinic acid supplementation of up to 100 mg/day in 21 healthy
smokers failed to provide any evidence of a decrease in cigarette smoke-induced
genetic damage in blood lymphocytes compared to placebo (15).
Generally, relationships between dietary factors and cancer are established
first in epidemiological studies and followed up by basic cancer research at the
cellular level. In the case of niacin, research on biochemical and cellular
aspects of DNA repair has stimulated an interest in the relationship between
niacin intake and cancer risk in human populations (16).Recently, a large
case-control study found increased consumption of niacin, along with antioxidant
nutrients, to be associated with decreased incidence of oral (mouth), pharyngeal
(throat), and esophageal cancers in northern Italy and Switzerland (17, 18). An
increase in niacin intake of 6.2 mg was associated with about a 40% decrease in
cases of cancers of the mouth and throat, while a 5.2 mg increase in niacin
intake was associated with a similar decrease in cases of esophageal cancer.
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