http://www.precaution.org/lib/08/ht080918.htm
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Rachel’s Democracy & Health News #977
“Environment, health, jobs and justice–Who gets to decide?”
Thursday, September 18, 2008…………Printer-friendly version
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Featured stories in this issue…
“Ask why diabetes is epidemic in the 21st century and most people
will point the finger at bad diet, laziness and obesity. According to
a small but growing group of scientists, though, the real culprit is a
family of toxic chemicals known as persistent organic pollutants, or
POPs… including dioxins, DDT and PCBs….”
Women who had been exposed to PCB-laced oil were twice as likely as
other women to develop type 2 diabetes over 24 years. And women who
had been most severely affected by the PCB exposure had a more than
five-times higher diabetes risk.
Dr. Pete Myers, chief scientist at the US-based Environmental
Health Sciences, said: “This is very important. It is the first good
study of the effects on the foetus. Its conclusions are not
surprising, given what we know from the animal experiments, but it
firmly links such chemicals to the biggest challenge facing public
health today.”
Is your baby drinking from a bottle made out of the common plastic
BPA? The U.S. Food and Drug Administration says it’s completely safe,
though other government agencies disagree. Now, for the first time,
we have direct evidence of human disease from exposure to BPA.
“More than 210 million litres of radioactive and chemical waste are
stored in 177 underground tanks at Hanford in Washington State. Most
are over 50 years old. Already 67 of the tanks have failed, leaking
almost 4 million litres of waste into the ground.”
Of the 704 species of corals that have been studied, scientists
say 32.8% are at risk of extinction. The fate of the other 141 coral
species remains unknown.
“The reality is we are stressing wildlife populations, killing them
through habitat loss and disease, and then also modifying them so they
cannot reproduce optimally.”
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From: New Scientist (pg. 36), Sept. 10, 2008
COULD THE DIABETES EPIDEMIC BE DOWN TO POLLUTION?
By Phyllida Brown
On July 10, 1976, a reactor at a chemical plant near the small town of
Seveso in northern Italy exploded, sending a toxic cloud drifting into
the summer sky. Around 18 square kilometres of land was contaminated
with TCDD, a member of the notorious class of industrial chemicals
known as dioxins.
The immediate after-effects were relatively mild: 15 children landed
in hospital with skin inflammation and around 3300 small animals were
killed. Today, however, the accident casts a long shadow over the
people of Seveso, who are suffering increased numbers of premature
deaths from cancer, cardiovascular disease and, perhaps surprisingly,
diabetes (American Journal of Epidemiology, vol 167, p 847).
To some diabetes researchers, Seveso serves as a warning to us all.
Ask why diabetes is epidemic in the 21st century and most people will
point the finger at bad diet, laziness and obesity. According to a
small but growing group of scientists, though, the real culprit is a
family of toxic chemicals known as persistent organic pollutants, or
POPs. If these researchers are right, POPs — which include some of
the most reviled chemicals ever created, including dioxins, DDT and
PCBs — may be key players in the web of events that lead people to
develop the disease.
The claim has yet to attract widespread attention from mainstream
diabetes research. Even its champions were initially surprised by it.
“I had never even heard of POPs until 2005,” says Duk-Hee Lee, an
epidemiologist at Kyungpook National University in Daegu, Korea, who
led the work. Lee and her co-workers are now convinced, albeit
reluctantly, that they are onto something. “The hypothesis is one that
I wish were not true,” says her colleague David Jacobs of the
University of Minnesota, Minneapolis.
Diabetes, and particularly its commonest form, type 2 (see “Sidebar:
Diabetes basics”), is practically everyone’s business. The World
Health Organization estimates that it already affects 180 million
people worldwide, with the number predicted to more than double by
2030. Last year the epidemic cost $174 billion in the US alone,
according to the American Diabetes Association.
========================================================
Sidebar: Diabetes basics
Diabetes has two main forms: type 1 and type 2. About 90 per cent of
diabetics have type 2.
Type 1 diabetes is an autoimmune disease in which insulin-producing
cells in the pancreas are progressively destroyed.
Type 2 diabetes usually develops in adulthood, although it is now
increasingly common in children. In this form, the pancreas either
produces too little insulin, or cells in the liver, muscles and fat
tissues fail to use it properly. Type 2 is most common in inactive,
overweight people who carry their fat on their midriff.
========================================================
The standard explanation for type 2 diabetes is that it is a
“lifestyle disease” caused by laziness and gluttony. For at least a
decade, however, epidemiologists have known that people briefly
exposed to high concentrations of POPs face a modest increase in their
risk of developing diabetes later in life. Those affected include the
people of Seveso and US veterans who were exposed to dioxin-
contaminated Agent Orange during the Vietnam war.
Two years ago, Lee, Jacobs and others decided to see whether everyday
exposure to POPs is also linked to diabetes. To their surprise and
horror, they found that it is.
For most people, POPs are inescapable: meat, fish and dairy products
all contain them. They enter the food chain from sources such as
pesticides, chemical manufacturing and incinerated waste, and
accumulate in animals higher up in the chain. Once in the body they
take up residence in fat.
POPs have long been recognised as nasty substances: their effects
include birth defects, cancer, immune dysfunction and endocrine
disruption. Since the 1970s, various measures have been put in place
to phase them out — 12 of the worst POPs, known as the “dirty dozen”,
were banned in 2004 — but despite these efforts, POPs remain a
significant presence in the environment and food chain, partly because
many are still in use in the developing world, and partly because
these chemicals can take decades to break down.
Role of fat
Prior to her 2005 introduction to POPs, Lee was working on a humble
enzyme called gamma-glutamyltransferase (GGT), which is essential for
maintaining antioxidant levels in the liver. She was puzzled to find
that obesity combined with an elevated level of GGT is a strong
predictor of diabetes, but obesity alone isn’t. “I searched the
literature and finally got an idea,” she says.
As it turns out, GGT has an essential role to play in removing some
pollutants, including POPs, from inside cells (Diabetologia, vol 51, p
402). Could increased GGT activity simply be a marker of exposure to
POPs?
To find out, Lee and her colleagues analysed data from more than 2000
people in the US National Health and Nutrition Examination Survey
(NHANES), which measured both diabetes status and bloodstream levels
of POPs, among other things. They discovered that people with high
levels of six different POPs in their bloodstream were much more
likely to have diabetes, regardless of obesity (see diagram). The six
POPs were chosen because they were detectable in at least 80 per cent
of the participants.
Taking into account factors such as weight, age, waist circumference
and ethnic group, Lee calculated that in people with the highest
combined levels of all six POPs the rate of diabetes was a massive 38
times greater than in those with the lowest levels (Diabetes Care, vol
29, p 1638). “The people who disagree with us will say it’s all
noise,” says Jacobs, “but it’s pretty hard to get odds ratios of 38
with noise.”
To her even greater surprise, Lee found that in people with
undetectable levels of POPs the expected link between diabetes and
body weight melted away — those who were obese were no more likely to
have diabetes than their lean counterparts. “This suggests that POPs
may be a more fundamental factor in the risk of diabetes than
obesity,” says Lee. “The absolute risk of diabetes was extremely low
among subjects with very low concentrations of POPs.”
“The expected link between diabetes and body weight melted away” But
fat is not off the hook just yet. While obesity alone appears not to
be linked with diabetes, the study suggests that POPs plus obesity is
bad news, and the fatter you are the worse it gets. When the
researchers examined the link with body mass index, they found that in
people with high levels of POPs the odds of being diabetic were much
higher for the obese than the lean. This suggests that something about
excess fat may be enhancing the toxicity of POPs. “It appears that
obesity can increase the harmful effects,” says Lee.
Of course, the findings do not prove that POPs cause diabetes. “This
is an association between two things, not direct evidence of a causal
link,” warns Oliver Jones, an environmental biochemist at the
University of Cambridge. The idea deserves further investigation,
though, he says.
Lee and her colleagues acknowledge that their interpretation could be
stood on its head. If diabetes causes the body to become less
efficient at dealing with POPs, then higher levels of POPs in people
with diabetes could be an effect of the disease, rather than its
cause. Lee does not rule out this possibility, but thinks it unlikely.
She points to a 2003 study by other researchers that found no
relationship between diabetes and the rate at which POPs are
eliminated from the body (Journal of Toxicology and Environmental
The team also examined the link between POPs and a metabolic disorder
called insulin resistance, in which muscle, fat and liver cells fail
to use insulin properly and which often progresses to full-blown
diabetes. Once again, they found that people whose blood contained the
highest levels of POPs were most likely to have insulin resistance
(Diabetes Care, vol 30, p 622). The results add weight to the idea
that POPs may be playing a vital role in the disease pathway from
insulin resistance to diabetes, says Lee. “I am really excited about
this.”
Even so, she acknowledges two obvious objections to her work. First,
while levels of POPs in the blood of Americans have been falling for a
couple of decades, the diabetes epidemic is just taking off. Lee
suggests that as obesity seems to make POPs more dangerous, its rising
prevalence may have cancelled out any health improvements that should
have followed the decline in POPs.
A second question is why, if POPs are central to diabetes, the
incidence of the disease is soaring not only in the meat-addicted west
but also in countries such as India, where many millions are
vegetarian. Lee’s answer is that, while many POPs are banned in the
west, some are still used as pesticides in developing countries. “The
highest rate of increasing risk of type 2 diabetes is observed in Asia
and Africa, not North America with the highest obesity rate,” she
says.
To try to slot POPs into the complex diabetes jigsaw, it is worth
taking a brief step into the mainstream to look at the role of fats,
or lipids, in the disease. Type 2 diabetes was once seen mainly as a
disorder of glucose metabolism. Now, says diabetes researcher Evan
Rosen of Beth Israel Deaconess Medical Center in Boston, the focus has
shifted, with many scientists considering that the primary problem
lies with the metabolism of fats.
For years, physiologists largely ignored fat cells, or adipocytes,
seeing them as little more than passive energy silos. Recently,
though, they have been revealed for what they are: highly active in
producing both hormones that regulate energy, and inflammatory
messenger chemicals that are important to the immune system (New
Scientist, 16 September 2000, p 36). If adipocytes malfunction, the
consequences can be widespread.
When we eat energy-rich foods, our bodies have to store any excess
energy not burned up by physical activity. Most is stored as fat in
adipocytes, but when these eventually fill up, excess lipid spills
over into other tissues, particularly the liver, muscles and the area
around the heart. The presence of this “ectopic fat” has been linked
to all sorts of health problems, including insulin resistance and
diabetes.
Just how might ectopic fat help to trigger diabetes, though? There is
no simple answer and researchers still disagree about the possible
mechanism. However, there are some clues.
In animals ectopic fat is known to attract the attention of the immune
system, which produces inflammatory messenger chemicals around it as
though it were an infection. Interestingly, people with diabetes have
chronically raised levels of these inflammatory chemicals, raising the
question of whether inflammation caused by ectopic fat could be a
factor in the disease.
Ectopic fat also causes problems when muscle cells try to burn it to
generate energy. In obese people this is a highly inefficient process,
probably because their mitochondria — the cell’s power plants –
function at a reduced capacity, says Rosen. Mitochondria in muscle
cells are already known to work less efficiently in people with
diabetes, and this year a team at Helsinki University Central Hospital
in Finland found similar changes in obese people with no symptoms of
diabetes (American Journal of Physiology — Endocrinology and
Metabolism, vol 295, p E148).”You end up with a half-burned lipid,”
says Rosen.
He speculates that this half-burned lipid acts like a magnet for
reactive oxygen species (ROS), including free radicals and peroxides,
which then inflict damage to the muscle cells themselves. There is now
clear evidence that chronic damage from ROS — known as oxidative
stress — helps to drive cells into insulin resistance. “If you block
ROS, you can block insulin resistance,” says Rosen.
If Lee is right, however, and POPs are at the root of diabetes, these
ideas tell only half the story. So how might POPs be involved? Again,
there are tantalising hints. Jones points out that POPs are known to
bind to a family of receptors on cell nuclei known as PPARs. These are
involved in lipid metabolism and are known not to work properly in
people with diabetes; the diabetes drug troglitazone works by
activating one member of the family, PPAR-gamma. People with an
inherited disorder of this receptor are unusually prone to insulin
resistance. Another intriguing link is that POPs are known to cause
mitochondrial dysfunction, which some researchers think is the root
cause of diabetes (Science, vol 307, p 384).
But none of this explains how POPs interact with obesity. It may be
that obese people simply have a higher load of POPs in their bodies.
Another possibility is that POPs in ectopic fat are particularly
dangerous. Perhaps, speculates Lee, adipocytes are a relatively safe
storage site for POPs. “Our body has to find some place to store
them,” she says, “and in this sense, adipose tissue is a relatively
safe organ.” The trouble might start when POP-contaminated ectopic fat
starts to build up in the muscles and liver, exposing the organs to a
direct toxic assault. “That way, the harmful effects of POPs could
become more serious,” Lee suggests.
Clearly more work is needed to establish the precise link between POPs
and diabetes. For Jones, it is surprising that Lee’s research has
remained relatively neglected, especially given its public health
implications. He does note, though, that other teams are starting to
investigate the hypothesis. Julian Griffin and others at Cambridge
have found that low-level mixtures of POPs can cause metabolic
disturbances similar to those seen in type 2 diabetes.
Rosen stresses that the lack of attention given to this research
should not be seen as an indictment of the work, but instead reflects
how deeply scientists specialise in their own areas. “We generally
stay inside our silos,” he says. “It’s incredibly difficult to move
outside of them.” Another problem, says Jacobs, is that testing the
hypothesis to destruction would require complex and long-term studies
of the type that funding bodies are often reluctant to commit money
to.
If Lee is right, it is not good news for the diabetes epidemic. Even
though many POPs are being phased out, they will take decades to clear
from the food chain. Meanwhile, newer POPs such as brominated flame
retardants continue to be manufactured in large quantities.
There is perhaps one silver lining. If you need an extra incentive to
stay lean, eat less meat and keep active, then knowing that toxic
chemicals lurking in your body fat could be a sure route to diabetes
might just be the motivation you’re looking for.
==============
Phyllida Brown is a writer based in Exeter, UK
Copyright Reed Business Information Ltd.
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From: Reuters health, Aug. 15, 2008
HIGH PCB EXPOSURE TIED TO DIABETES RISK
NEW YORK (Reuters Health) — People who have been exposed to high
levels of toxic polychlorinated biphenyls (PCBs) may face an elevated
risk of type 2 diabetes, a new study shows.
The findings, reported in the journal Diabetes Care, come from a
long-term study of Taiwanese adults who, in the 1970s, had been
poisoned by cooking oil contaminated with PCB pollutants.
Once used in products ranging from fluorescent lights and appliances
to insulation and insecticide, PCBs were banned in the late 1970s as
carcinogens and general health hazards. They linger in the
environment, however.
In the new study, Dr. Yueliang Leon Guo, from the National Taiwan
University in Taipei, and colleagues examined the incidence of type 2
diabetes among 378 Taiwanese “oil disease” victims and 370 of their
neighbors who had not been poisoned.
They found that women who had been exposed to the PCB-laced oil were
twice as likely as other women to develop type 2 diabetes over 24
years. And women who had been most severely affected by the PCB
exposure had a more than five-times higher diabetes risk.
There were no similar risks seen in men, however.
Other studies have found that people with diabetes tend to have
relatively higher levels of organic pollutants, such as PCBs, in their
blood. In comments to Reuters Health, Guo said that since “everyone”
has detectable PCB levels in his or her body, it’s possible that
exposure to such pollutants has helped feed the widespread rise in
diabetes in recent decades.
“The public health implication of these findings can be huge,” Guo
added, “considering the burden of diabetes and its multiple long-term
complications.”
SOURCE: Diabetes Care 2008, August 2008.
Copyright 2008 Reuters Limited
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From: The Telegraph (London, U.K.), Sept. 9, 2008
POLLUTION LINKED TO OBESITY, NEW STUDY FINDS
By Chris Irvine
Pollution could determine whether a child is fat or not before they
have even been born, a new study has found.
Exposure to a range of common chemicals before birth increases the
chance of a baby to growing up overweight or obese, the research
indicates.
The study by scientists at Barcelona’s Municipal Institute of Medical
Research is the first to link obesity with chemical contamination in
the womb, where humans are most vulnerable.
A quarter of all British adults and a fifth of children suffer from
obesity, with at least 300 million obese worldwide.
Published in the current issue of the journal Acta Paediatrica, the
research measured levels of hexachlorobenzene (HCB) in the umbilical
cords of 403 children born on the Spanish island of Menorca.
HCB is a pesticide banned internationally but which continues to
remain in the environment and can be found in food.
Those with the highest levels of HCB were twice as likely to be obese
when they reached the age of six and a half.
The report’s authors are now calling for exposure to similar
pesticides to be minimised, including bisphenol A (BPA), used in baby
bottles and cans of food, and phthalates, found in cosmetics and
shampoos.
Tests have shown BPA is found in 95 per cent of Americans, while 90
per cent have been found to be exposed to phthalates in the womb.
Dr Pete Myers, chief scientist at the US-based Environmental Health
Sciences, said: “This is very important. It is the first good study of
the effects on the foetus. Its conclusions are not surprising, given
what we know from the animal experiments, but it firmly links such
chemicals to the biggest challenge facing public health today.”
The research comes after Conservative leader David Cameron said that
obesity is purely a matter of “personal responsibility”.
Copyright of Telegraph Media Group Limited 2008
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From: Reuters, Sept. 16, 2008
COMMON PLASTICS CHEMICAL LINKED TO HUMAN DISEASES
London, Sept 16 — A study has for the first time linked a common
chemical used in everyday products such as plastic drink containers
and baby bottles to health problems, specifically heart disease and
diabetes.
Until now, environmental and consumer activists who have questioned
the safety of bisphenol A, or BPA, have relied on studies showing harm
from exposure in laboratory animals.
But British researchers, who published their findings on Tuesday in
the Journal of the American Medical Association, analyzed urine and
blood samples from 1,455 U.S. adults aged 18 to 74 who were
representative of the general population.
Using government health data, they found that the 25 percent of people
with the highest levels of bisphenol A in their bodies were more than
twice as likely to have heart disease and, or diabetes compared to the
25 percent of with the lowest levels.
“Most of these findings are in keeping with what has been found in
animal models,” Iain Lang, a researcher at the University of Exeter in
Britain who worked on the study, told a news conference.
“This is the first ever study (of this kind) that has been in the
general population,” Lang said.
Steven Hentges of the American Chemistry Council, a chemical industry
group, said the design of the study did not allow for anyone to
conclude BPA causes heart disease and diabetes.
“At least from this study, we cannot draw any conclusion that
bisphenol A causes any health effect. As noted by the authors, further
research will be needed to understand whether these statistical
associations have any relevance at all for human health,” Hentges said
in a telephone interview.
A U.S. Food and Drug Administration panel of outside experts on
Tuesday will hear testimony on health effects from BPA as it reviews a
draft report it issued last month calling BPA safe.
“The study, while preliminary with regard to these diseases in humans,
should spur U.S. regulatory agencies to follow recent action taken by
Canadian regulatory agencies, which have declared BPA a ‘toxic
chemical’ requiring aggressive action to limit human and environmental
exposures,” Frederick vom Saal of the University of Missouri and John
Peterson Myers of the nonprofit U.S.-based Environmental Health
Sciences, wrote in a commentary accompanying the study.
BOTTLES TO UTENSILS
BPA is used to make polycarbonate plastic, a clear shatter-resistant
material in products ranging from baby and water bottles to plastic
eating utensils to sports safety equipment and medical devices.
It also is used to make durable epoxy resins used as the coating in
most food and beverage cans and in dental fillings.
People can consume BPA when it leaches out of plastic into liquid such
as baby formula, water or food inside a container.
In the study, the team said the chemical is present in more than 90
percent of people, suggesting there is not much that can be done to
avoid the chemical of which over 2.2 million tonnes is produced each
year.
The researchers, who will also present their findings at the U.S. FDA
session on Tuesday, added it was too early to identify a mechanism
through which the chemical may be doing harm.
Animal studies have suggested the chemical may disrupt hormones,
especially estrogen.
The researchers also cautioned that these findings are just the first
step and more work is needed to determine if the chemical actually is
a direct cause of disease.
“Bisphenol A is one of the world’s most widely produced and used
chemicals, and one of the problems until now is we don’t know what has
been happening in the general population,” said Tamara Galloway, a
University of Exeter researcher who worked on the study.
Canada’s government in April decided BPA was harmful to infants and
toddlers and announced plans to ban some products.
The European Union’s top food safety body said in July the amount of
BPA found in baby bottles cannot harm human health.
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From: New Scientist (pg. 7), Jul. 14, 2008
CONTAMINATED U.S. SITE FACES ‘CATASTROPHIC’ NUCLEAR LEAK
One of “the most contaminated places on Earth” will only get dirtier
if the US government doesn’t get its act together — clean-up plans
are already 19 years behind schedule and not due for completion until
2050.
More than 210 million litres of radioactive and chemical waste are
stored in 177 underground tanks at Hanford in Washington State. Most
are over 50 years old. Already 67 of the tanks have failed, leaking
almost 4 million litres of waste into the ground.
There are now “serious questions about the tanks’ long-term
viability,” says a Government Accountability Office report [2.1
Mbytes PDF], which strongly criticises the US Department of Energy
for delaying an $8 billion programme to empty the tanks and treat the
waste. The DoE says the clean-up is “technically challenging” and
argues that it is making progress in such a way as to protect human
health and the environment.
The DoE’s plan, however, is “faith-based”, says Robert Alvarez, an
authority on Hanford at the Institute for Policy Studies in Washington
DC. “The risk of catastrophic tank failure will sharply increase as
each year goes by,” he says, “and one of the nation’s largest rivers,
the Columbia, will be in jeopardy.”
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From: New Scientist, Jul. 10, 2008
CORALS JOIN FROGS AND TOADS AS WORLD’S MOST ENDANGERED
By Catherine Brahic
Within one generation, diving on coral reefs could be a very rare
holiday opportunity. The first comprehensive review of tropical coral
species reveals that over one-quarter reef-building coral species
already face extinction.
This means corals join frogs and toads as the most threatened group of
animal species on the planet.
There are 845 known species of corals that build reefs and live in
symbiosis with algae. Not enough is known about 141 of these to
determine how threatened they are. But of the 704 remaining species,
scientists say 32.8% are at risk of extinction.
The team, which was led by Kent Carpenter of the International Union
for the Conservation of Nature (IUCN) and gathered experts from around
the world, used the IUCN Red List criteria to assess the 845 species.
Sewage and climate
Two hundred and thirty one species (27%) were found to be threatened
with extinction. A further 176 (21%) were deemed “near-threatened”.
“It was a huge surprise because there is only one other group of
animals that has been assessed that exceed that level of threat,” says
Alex Rogers of the Zoological Society of London, who participated in
the survey, “and that’s the amphibians.”
Humans directly threaten corals by dumping fertilisers and sewage into
the oceans and by overfishing with destructive methods.
All this encourages the growth of larger algae, which smother corals.
“Outside of the US and Europe, 80% of human sewage is released into
the oceans without treatment,” says Rogers.
Global warming increases sea temperatures which causes “bleaching”
events, where the reefs expel the tiny algae upon which they depend.
Warming has also been associated with an increased incidence of coral
diseases.
Large-scale disaster
In 1998, a world-wide coral bleaching triggered by unusually warm seas
irreversibly destroyed 16% of the coral reef area worldwide.
Coral reefs are home to 25% of all fish species, and as many as 2
million species of animals and plants.
In this sense, they are the tropical rainforests of the oceans and the
1998 bleaching event can be compared to irreversibly wiping out 240
million hectares of forest — equivalent to half of the Amazon.
“If this happened in terrestrial ecosystems we would all be shouting
from the treetops,” says Rogers. “And yet, it has now completely
passed out of public memory.”
Valuable resource
“I have two children that are under one-and-a-half years old. I expect
that by the time they are 40, coral reefs will have massively declined
and in some regions, such as the Caribbean, they will be pretty much
gone. By the end of the century there could be virtually nothing
left.”
Conserving corals will require doing more than addressing the causes
of climate change, but the benefits will be considerable. Reef fish
feed more than 1 billion people in the developing world and the
overall value of coral reefs is estimated at more than $30 billion a
year.
There is a little good news, though. The 1998 bleaching event revealed
that some species of corals appear to be resistant to coral bleaching,
suggesting that these species may become hardy survivors.
Restored reefs
At the 11th International Coral Reef Symposium held in Florida this
week, a team of scientists presented evidence that some strains of the
endangered staghorn coral Acropora cervicornis can resist white band
disease.
This disease has caused mass die-offs of staghorn corals in the
Caribbean, resulting in them being listed in the US Endangered Species
Act. The researchers say the findings suggest it might be possible to
propagate resistant strains to restore the endangered reefs.
Recent studies have highlighted the plight of coral reefs in different
areas around the world. In 2007, researchers announced that reefs in
the Pacific are disappearing twice as fast as tropical rainforests.
And in 2003, another team showed that Caribbean corals were
dangerously close to extinction.
Journal reference: Science (DOI: 10.1126/science.1159196)
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From: Environmental Health News, Sept. 15, 2008
FEMINIZED TOADS LINKED TO FARMS.
Toads living in agricultural areas of Florida are more likely to be
feminized than their suburban counterparts.
By Marla Cone, Editor in Chief
Along the shore of Florida’s Lake Okeechobee, male toads seem more
like females. Most have ovaries as well as testes, the mottled skin of
a female and depleted testosterone.
Nearby, in a Palm Beach suburb, the toads are normal. The difference?
The feminized ones live in areas with heavy agriculture while the
normal males inhabit suburban areas.
Scientists at University of Florida have documented that proximity to
farms increases the chances that amphibians are half-male, half
female. The more intense the agriculture, the more feminized the male
toads, and the more likely they can’t reproduce.
The new findings intensify the already highly contentious debate over
whether pesticides — particularly atrazine, one of the most widely
used herbicides in the United States — are messing up the
reproductive organs of wildlife.
Some scientists say that pesticide exposure is likely to be a big
piece of a puzzle that they have tried to solve for decades: What is
wiping out frogs and amphibians around the world?
Louis Guillette The threat from agriculture “is part of a complex
response that endangers frog and other wildlife populations,” said
Louis Guillette, senior author of the study and a University of
Florida Distinguished Professor of Zoology.
You have stacked the deck against healthy populations,” he said. “The
reality is we are stressing wildlife populations, killing them through
habitat loss and disease, and then also modifying them so they cannot
reproduce optimally.”
The new research “adds to the support that agriculture causes these
problems,” said Tyrone Hayes, a professor of integrative biology at
University of California at Berkeley.
Hayes in 2003 published data that showed frogs exposed in the
laboratory to the herbicide atrazine became hermaphroditic.
However, other studies, many of them industry-funded, have found no
such effects. The U.S. Environmental Protection Agency concluded last
year after a review of existing data that there was insufficient data
to suggest that atrazine feminizes amphibians. Its science advisory
committee agreed.
Dr. Tim Pastoor, principal scientist at Syngenta, the manufacturer of
atrazine, said “a growing body of research conducted by independent
labs across the world is showing that atrazine does not affect the
sexual development of amphibians.”
Florida’s gender-bending chemicals
University of Florida’s research in the early 1990s, led by Guillette,
was considered pivotal science that led to worldwide concern about
chemicals that mimic or block hormones. The scientists linked the
pesticide dicofol, which contains DDT, to feminized alligators in
Florida’s Lake Apopka. The phenomenon, called endocrine disruption,
has now been replicated in research on various species and chemicals
throughout the world.
In the new study, scientists collected toads from five sites in South
Florida. At the two places, Belle Glade and Canal Point, where most
land is farmed, about 60% of males had feminized sex organs, including
35% to 40% that were considered intersex, with both ovaries and
testes. But at Lake Worth, which has no agriculture, there were no
intersex toads and feminized traits were found in less than 10%.
Also, the male toads in the agricultural areas had fewer pads on their
thumbs which grow on mating males. Their testosterone levels were low
in the farmed areas, similar to those of female toads.
Andrew Blaustein, a zoology professor at Oregon State University who
studies environmental threats to frogs, said the more-subtle, feminine
changes found in the males — particularly the lack of thumb pads
allowing them to hold on to a mate–could have dramatic effects on
their ability to breed.
“The secondary sexual traits are really striking,” he said.
Although the new study only looked at cane toads, which are not native
to Florida, “we have also studied green tree frogs and southern toads,
and both show similar gonadal abnormalities at the agricultural
sites,” said Krista McCoy, lead author of the Florida study, which was
published in an online edition of Environmental Health Perspectives in
July.
“In general amphibian reproductive system development is very
sensitive to hormones, natural and man-made,” McCoy said. As a result,
she said “what we find in cane toads is likely occurring in other
species and might be contributing to their rarity.”
Effects on specific populations, however, have not been documented.
Scientists do not know whether any hormone-mimicking pesticides have
caused population declines in amphibians
“We know that many pollutants are distributed globally, and we know
that amphibian populations are declining globally, faster than birds
or mammals actually. But we do not have an understanding of the role
that pollutants are playing in amphibian population declines,” McCoy
said.
Across all species, hormone systems are strikingly similar, regulating
how the reproductive tract develops. Scientists suspect that the same
chemicals that feminize toads might be feminizing human boys, too.
“In fact, there is general concern among scientists who study
endocrine disrupting chemicals that some of the very chemicals used at
the agricultural sites we studied are negatively affecting humans,”
McCoy said.
‘The big suspect is atrazine’
About 888 million pounds of active pesticide ingredients were used in
2001, 76% for agriculture, according to EPA data. Of that, 550 million
pounds were herbicides. Corn is the major crop using herbicides,
accounting for more than one-third of the total. Illinois and Iowa
lead the nation in herbicide use.
The Florida team did not implicate any particular chemical. But the
primary pesticide used in that area is atrazine, applied to sugarcane
fields.
“The big suspect is atrazine,” Hayes said. “What makes atrazine
particularly bad is that it is everywhere. It is the one pesticide
that’s always there, that’s persistent. There is no other evidence at
this point for other pesticides.”
Hayes theorizes that atrazine feminizes animals by activating an
enzyme that causes an imbalance between testosterone and estrogen.
“We have effects in fish, and similar effects in alligators and other
species, and we have studies on human cell lines,” Hayes said. “To me
it’s a no-brainer. That can’t be a coincidence.”
However, the EPA mounted a review of 19 laboratory and field studies
exploring the effects on amphibians, and concluded last year that
atrazine does not feminize them.
Syngenta’s Pastoor said the new study “contains major uncertainties
that render the data interpretation unreliable.” For example, the age
of the toads was not reported, and that is important because sexual
characteristics vary with age, he said.
While atrazine is used in South Florida, concentrations in water near
the places where the toads were collected “are extremely low,” Pastoor
said.
Some scientists, however, say there is ample evidence that pesticides
are harming frogs and related animals. Hayes has criticized the EPA
for relying too heavily on studies conducted by atrazine’s
manufacturer.
Said Blaustein, the Oregon State zoology professor: “Not only can
these pesticides have direct effects, they can have indirect effects.
They can kill you, they can screw up your physiology and anatomy and
they can put you under stress and hamper your immune systems, so they
are nasty.”
Throughout much of the world, urban development, introduced predators
and diseases all play a role in the disappearance of native frogs,
toads and other amphibians.
Diseases and parasites have killed many amphibians, but immune-
suppressing chemicals might contribute to those deaths.
“In some ways it is the AIDS story,” Guillette said. “If you have
reduced immune function you increase the chance of having a full blown
infection that then sets you up for every other pathogen you come in
contact with.”
Copyright 2003 Environmental Health Sciences
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