[All] APTN Environmental TV Series Begins Today
Susan Koswan
dandelion at gto.net
Tue Mar 9 08:54:07 EST 2010
FYI,
For your reading and viewing pleasure for those with a particular interest
in the effects of pollution (POPS) and the onset of diabetes.
Susan K
-----Original Message-----
From: John Hummel [mailto:jhwhummel at shaw.ca]
Sent: March-08-10 2:56 PM
To: Get Rid of Urban Pesticides
Subject: [OEN referral] Alert! APTN Environmental TV Series Begins Today
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
[this message is a referral through the Ontario
Environmental Directory http://www.oen.ca/dir/
(please report any abuse to oen at oen.ca )]
~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~~
Dear Friends,
Here is information on some important environmental programs starting
today, Monday March 8th on the Aboriginal People's Television Network
(APTN). Also, I have included recent information on the connection
between pollution exposure (particularly pesticides) and the onset of
diabetes as well as contacts and tools to do something about all this.
Please share this information very widely with all your contacts (both
allies and media). All the best to you.
For Land and Life,
John H.W. Hummel,
Volunteer Pollution/Health Researcher,
Nelson, B.C.
"APTN BRINGS VIEWERS “PERSPECTIVES ON THE ENVIRONMENT”
March 1, 2010 - APTN National News will premiere Perspectives on the
Environment, a week dedicated to environmental issues affecting
communities across Canada. The stories, which will be featured during
APTN National News March 8 to March 11 at 6:00 pm ET on APTN East/MT
on APTN West/CT on APTN North/ET on APTN HD, and will culminate in an
hour-long special season finale edition of APTN InFocus March 12, will
focus on the major issues in every region of Canada: North,
South/Central, East and West.
“APTN National News is devoted to bringing viewers the stories
affecting our communities,” said Sky Bridges, Director of Marketing.
“People are exposed to media coverage on environmental issues daily;
Perspectives on the Environment will make specific issues and
realities known and truly reveal how these problems are affecting the
well-being, spirit, and future of not only Aboriginal Peoples but all
Peoples.”
APTN Environmental Week Outline:
North – Peel Watershed – airdate Monday March 8th:
The Yukon’s Peel Watershed is rich in minerals and other resources,
but many of the people who use the Peel Watershed say it’s worth
protecting from development. APTN’s Dez Loreen will look at the
resources that make the land so valuable, the traditions that make the
region so rich, and the debate over how best to deal with it all.
East – Boat Harbour, Nova Scotia – airdate March 9th:
The Pictou Landing First Nation has been fighting for more than 40
years to get the Nova Scotia government and industry to clean up the
harbour. The waters, which at one time featured pristine beaches, are
now making people sick. Nova Scotia Premier Darrell Dexter’s new NDP
government says it’s committed to solving the Boat Harbour problem.
APTN’s James Hopkin talks to the people in the Mi’kmaq community and
to the 10th provincial minister to deal with the file.
South/Central – Mercury Pollution airdate March 10th:
The people of the Grassy Narrows First Nation in Ontario are battling
the severe health effects of mercury exposure. The emissions that
polluted the watershed where they live began decades ago and the
federal government says the problem has been fixed, but young people
in the community are still showing the horrific symptoms of mercury
poisoning. APTN's Melissa Ridgen visited the community to find answers.
West – Deep Water Port for Super Tankers airdate March 11th:
Plans are in development for a pipeline to carry oil from the Alberta
tar sands to Kitimat, British Columbia, where a deep water port will
provide transport to supertankers which will carry oil to US and
Pacific Rim markets. The ships will navigate near Hartley Bay First
Nation, one of the country’s most environmentally conscious
communities. With the nearby waters being well-known for their danger,
the people of Hartley Bay fear a massively destructive oil spill.
APTN's Noemi LoPinto travels to the community to find out what happens
next.
APTN InFocus One-Hour Season Finale airdate March 12th:
· On Friday, March 12th APTN National News will be pre-empted
for a special one-hour edition (and season finale) of APTN InFocus.
This special edition will feature a panel of experts who will discuss
the four Perspectives on the Environment stories that aired during the
week on APTN National News.
They will also examine the poor water quality in many Indigenous
communities, 119 of which are under a Drinking Water Advisory.
The panel of experts will include:
Dr. John O’Connor, the physician who blew the whistle on unusually
high incidence of cancer clusters near the Alberta oil patch (Fort
McMurray).
Merrell-Ann S. Phare, Executive Director and Legal Counsel, Centre for
Indigenous Environmental Resources.
Ramsay Hart, Canada Program Coordinator, Mining Watch Canada, to deal
with environmental aspects of mining
Dr. Shirley Thompson, University of Manitoba, Assistant Professor,
Natural Resources Institute, will talk about the actual biological
effects of industrial pollution on the human body.
APTN National News is part of an exciting programming schedule that
promotes and celebrates Canadian content across all genres. Providing
news that not only informs, but inspires, APTN National News brings
viewers a more in-depth look at the issues facing Aboriginal
communities in Canada and around the world.
About APTN:
September 1, 2009 marked the 10-year anniversary of the launch of the
first national Aboriginal television network in the world with
programming by, for and about Aboriginal Peoples to share with all
Canadians and viewers around the world. APTN is available in
approximately 10 million Canadian households and commercial
establishments with cable, direct-to-home satellite (DTH),
telco-delivered and fixed wireless television service providers. The
network launched its high definition channel APTNHD in the spring of
2008. APTN does not receive government funding for operations but
generates revenue through subscriber fees, advertising sales and
strategic partnerships. APTN broadcasts programming with 56% offered
in English, 16% in French and 28% in Aboriginal languages. For program
schedule or for more information, please contact APTN at (204)
947-9331 or toll-free at 1-888-278-8862, or visit the website at
www.aptn.ca.
APTN PROPOSE « PERSPECTIVES ON THE ENVIRONMENT »
APTN National News présente en première « Perspectives on the
Environment », une semaine consacrée aux problèmes environnementaux
qui frappent des collectivités de tout le Canada. Les reportages
seront diffusés entre les 8 et 11 mars pendant le bulletin APTN
National News de 18 h, HE, sur APTN Est / HR, sur APTN Ouest / HC sur
APTN Nord / HE, sur APTN HD, et ils mèneront le 12 mars à un spécial
d’une heure qui marquera la fin de la saison d’APTN InFocus. Il y sera
question des principaux enjeux de chacune des régions du pays, soit le
Nord, le Centre-Sud, l’Est et l’Ouest.
« APTN National News s’emploie à présenter aux téléspectateurs des
sujets qui touchent nos collectivités », a déclaré Sky Bridges,
directeur du marketing. « Les gens sont exposés à une couverture
médiatique quotidienne des questions environnementales; « Perspectives
on the Environment » fera connaître des problèmes et des réalités
précis, et dévoilera comment ces problèmes nuisent au bien-être, à
l’esprit et à l’avenir non seulement des peuples autochtones, mais
aussi de tous les peuples. »
Grandes lignes de la Semaine de l’environnement d’APTN :
Nord – Bassin versant de la Peel – diffusé le lundi 8 mars :
Le bassin versant de la Peel, au Yukon, est riche en minéraux et en
autres ressources. Toutefois, bon nombre de ses utilisateurs affirment
qu’il vaut la peine de le préserver du développement. Dez Loreen, de
l’équipe d’APTN, étudiera les ressources qui rendent la terre aussi
précieuse, les traditions qui enrichissent autant la région, et le
débat au sujet de la meilleure façon de régler la situation.
Est – Boat Harbour, Nouvelle‑Écosse – diffusé le 9 mars :
La Première Nation de Pictou Landing se bat depuis plus de 40 ans pour
obtenir du gouvernement de la Nouvelle‑Écosse et du secteur privé
qu’ils nettoient le port. Les eaux, dont les plages étaient autrefois
en parfaite condition, sont aujourd’hui porteuses de maladies. Le
premier ministre de la Nouvelle‑Écosse, Darrell Dexter, qui est à la
tête du nouveau gouvernement démocrate, dit qu’il entend régler le
problème de Boat Harbour. James Hopkin, de l’équipe d’APTN,
s’entretient avec les membres de la collectivité mi’kmaq et avec le
10e ministre provincial saisi du dossier.
Centre-Sud – Pollution au mercure – diffusé le 10 mars :
Les membres de la Première Nation de Grassy Narrows, en Ontario,
luttent pour contrer les graves effets sur la santé de l’exposition au
mercure. Les émissions ont commencé à polluer leur bassin versant il y
a des décennies, et le gouvernement fédéral soutient que le problème a
été réglé. Pourtant, les jeunes de la collectivité continuent
d’afficher les horribles symptômes de l’empoisonnement au mercure.
Melissa Ridgen, de l’équipe d’APTN, se rend dans la collectivité pour
trouver des réponses.
Ouest – Port en eau profonde pour gros navires-citernes – diffusé le
11 mars :
Des projets en cours d’élaboration visent la construction d’un
pipeline qui acheminera le pétrole depuis les sables bitumineux de
l’Alberta jusqu’à Kitimat, en Colombie‑Britannique, où un port en eau
profonde permettra le transport du pétrole par gros navires-citernes
vers les marchés des États-Unis et de la côte du Pacifique. Les
navires passeront près de la Première Nation de Hartley Bay, une des
collectivités les plus sensibilisées à l’environnement au pays.
Puisque la dangerosité des eaux environnantes est bien connue, les
gens de Hartley Bay craignent un déversement de pétrole très
destructeur. Noemi LoPinto, de l’équipe d’APTN, visite la collectivité
pour connaître la suite des choses.
Spécial d’une heure – Dernière de la saison d’APTN InFocus – diffusé
le 12 mars :
· Le vendredi 12 mars, APTN National News cédera la place à
une émission spéciale d’une heure (dernière de la saison) d’APTN
InFocus. Cette émission spéciale fera appel à un groupe d’experts qui
discutera des quatre reportages diffusés au cours de la semaine
pendant le bulletin APTN National News, sous le thème « Perspectives
on the Environment ». En outre, il se penchera sur la mauvaise qualité
de l’eau au sein de nombreuses collectivités autochtones, dont 119
doivent observer un avis d’ébullition de l’eau.
Le groupe d’experts sera formé de :
John O’Connor, le médecin qui a dénoncé le nombre anormalement élevé
de grappes de cas de cancer près des champs de pétrole de l’Alberta
(Fort McMurray).
Merrell-Ann S. Phare, directrice générale et conseillère juridique,
Centre autochtone de ressources environnementales.
Ramsay Hart, coordonnateur du programme Canada, Mines Alerte Canada,
traitera des aspects environnementaux de l’exploitation minière.
Shirley Thompson, professeure adjointe au Natural Resources Institute
de l’Université du Manitoba, parlera des effets biologiques actuels de
la pollution industrielle sur le corps humain.
APTN National News s’inscrit dans une grille de programmation
emballante qui privilégie et célèbre un contenu canadien de tous
genres. En leur transmettant des nouvelles qui informent et inspirent,
APTN National News amène les téléspectateurs à poser un regard plus
approfondi sur les difficultés auxquelles les collectivités
autochtones du Canada et du reste du monde sont confrontées.
À propos d’APTN
Le 1er septembre 2009 a marqué le 10e anniversaire de l’entrée en
ondes d’APTN, le premier réseau national de télévision autochtone au
monde. Conçues par et pour les Autochtones et au sujet de ces
derniers, ses émissions s’adressent à tous les Canadiens et aux
téléspectateurs du monde entier. APTN est capté dans quelque 10
millions de foyers et d’établissements commerciaux au Canada, grâce à
la télévision par câble, à la diffusion directe, à la téléphonie et à
la technologie sans fil. Le Réseau a inauguré son canal à haute
définition APTN HD au printemps 2008. Les revenus d’APTN, qui ne
reçoit aucun financement d’exploitation du gouvernement, proviennent
des frais d’adhésion, de la vente de publicité et de partenariats
stratégiques. Sa programmation est diffusée à 56 % en anglais, à 16 %
en français et à 28 % dans des langues autochtones. Pour obtenir
l’horaire de programmation ou des renseignements supplémentaires,
veuillez communiquer avec APTN au 204-947-9331 ou, sans frais, au
1-888-278-8862, ou encore visitez le www.aptn.ca.
Paul Barnsley
Executive Producer - Investigative News
Aboriginal Peoples Television Network
339 Portage Avenue
Winnipeg, Manitoba R3B 2C3
P: 204.947.9331 ext. 327
F: 204.946.0767
C: 204.223.5614
Toll Free: 1.888.278.8862
pbarnsley at aptn.ca
www.aptn.ca
Canada's 4th National Broadcaster
Diabetes may be linked to pollutants
Published: Jan. 29, 2010 at 4:00 PM - UPI
WINNIPEG, Manitoba, Jan. 29 (UPI) -- There is growing evidence
diabetes -- especially among indigenous people -- may be linked to
environmental pollutants, U.S. and Canadian researchers say.
One-out-of-four indigenous adults living on reserves in Canada have
been diagnosed with type 2 diabetes, The Dominion reports.
More than a dozen published studies show a diabetes link to persistent
organic pollutants, including polychlorinated biphenyls, carcinogenic
hydrocarbons, or dioxins and synthetic pesticides such as DDT.
Environment Canada's National Pollutant Release Inventory says there
are 212 indigenous communities in Canada living near or downstream
from pulp mills and other facilities that produce dioxins and furans.
In 2006, Dr. Duk-Hee Lee and colleagues found people with the highest
rate of exposure to persistent organic pollutants were roughly 38
times more likely to have diabetes than those with the lowest rate of
exposure.
However, people who were obese but did not have high levels of
persistent organic pollutants were not at increased risk of developing
diabetes.
A 1994 draft report by the U.S. Environmental Protection Agency, which
has never been formally released to the public, says 93 percent of
exposure to dioxin comes from the consumption of beef, dairy, milk,
chicken, pork, fish and eggs, The Dominion says.
Bitter Sweet or Toxic? Indigenous people, diabetes and the burden of
pollution
There may be more to diabetes than our diet, or whether or not we get
enough exercise. According to several new studies, it may be the
result of our exposure to Persistent Organic Pollutants.
Note: this is a revised version of my article, “Bitter Sweet or
Toxic?” featured in this month’s issue of the Dominion, February 2010.
Link to this article which includes hyperlinks to all the relevant
documents:
http://intercontinentalcry.org/indigenous-people-diabetes-and-the-burden-of-
pollution/
Bitter Sweet or Toxic?
Indigenous people, diabetes and the burden of pollution
WINNIPEG—Diabetes is now widely regarded as the 21st century epidemic.
With some 284 million people currently diagnosed with the disease,
it’s certainly no exaggeration—least of all for Indigenous people.
According to the State of the World’s Indigenous Peoples Report by the
United Nations, more than 50 per cent of Indigenous adults over the
age of 35 have Type 2 Diabetes, “and these numbers are predicted to rise.”
Diabetes is referred to as a “lifestyle disease,” its rampant spread
believed to be caused by obesity due to our increased reliance on the
western diet (also known as the “meat-sweet” diet) and our avoidance
of regular exercise.
While these may certainly be contributing factors, there is growing
evidence that diabetes is closely linked with our environment.
More than a dozen studies have been published that show a connection
between Persistent Organic Pollutants (POPs) including polychlorinated
biphenyls (PCBs); carcinogenic hydrocarbons known as Dioxins; and the
“violently deadly” synthetic pesticide, DDT and higher rates of the
disease.
“If it is the POPs, not the obesity that causes diabetes, this is
really striking if true,” says Dr. David O. Carpenter, director of the
Institute for Health and the Environment at the University of Albany.
One out of four Indigenous adults living on reserves in Canada have
been diagnosed with Type 2 Diabetes, the most common form of diabetes.
The prevalence of the disease appears to be so great that the number
of new cases being diagnosed in Canada may exceed the growth of the
Indigenous population. It’s no longer uncommon to find children as
young as three with the disease.
According to government statistics, 27 per cent of all Indigenous
people in Canada will have Type 2 Diabetes in the next ten years.
Sandy Lake First Nation, in the Sioux Lookout Zone of northern
Ontario, has all but met the mark. A March 2009 study co-authored by
Dr. Stewart Harris found that 26 per cent of the community has the
disease, the highest recorded rate of diabetes in Canada. With a
population of 2,500, the northern Cree community was recently
described as an “epicentre” of the epidemic.
There has been little research on the levels of persistent organic
pollutants in Sandy Lake; however, according to the First Nations
Environmental Health Innovation Network, several neighboring
communities who also have high rates of diabetes, like
Kitchenuhmaykoosib Inninuwug First Nation, are known to have elevated
levels of PCBs in their blood.
The Mohawk community of Akwesasne has its own conflict with diabetes
and exposure to POPs. Located across the New York-Ontario-Quebec
borders along the St. Lawrence River, three aluminum foundries upriver
from the reserve dumped PCBs into the river for decades, contaminating
the water, soil, and vegetation.
For many years, Dr. Carpenter has been involved in the study of Adult
Mohawks at Akwesasne. Most recently, in 2007, he took part in a study
to examine the diabetes/pollution link in the community. “Our study of
adult Mohawks showed a striking elevation in rates of diabetes in
relation to blood levels of three persistent organic pollutants, DDE,
the metabolite of DDT, hexachlorobenzene and PCBs,” Dr. Carpenter
explains. “Our results are quite compatible with those of Lee et al.”
In 2006, Dr. Duk-Hee Lee and her colleagues showed that people with
the highest rate of exposure to POPs were roughly 38 times more likely
to have diabetes than those with the lowest rate of exposure. Further,
“they showed that people who were obese but did not have high levels
of POPs were not at increased risk of developing diabetes,” continues
Dr. Carpenter. “Probably the reason most people get obese is that they
eat too many animal fats, and this is where the POPs are.”
The dietary source of POPs was confirmed by the US Environmental
Protection Agency in their Draft 1994 Dioxin Reassessment, which has
never been formally released to the public. According to the Draft
Reassessment, 93 per cent of our exposure to Dioxin comes from the
consumption of beef, dairy, milk, chicken, pork, fish, and eggs; in
other words, the western diet.
A May 2001 study published in the Journal of Toxicology and
Environmental Health drew similar conclusions to the EPA Reassessment.
In addition, the study found that “nursing infants have a far higher
intake of dioxins relative to body weight than do all older age
groups,” and that human breast milk was twice as toxic as dairy milk.
It also found that vegans had the overall lowest rate of POPs in their
bodies.
According to an October 2009 paper by the Research Centre for
Environmental Chemistry and Ecotoxicology at Masaryk University,
another major source of POPs, specifically DDT, is the world’s oceans.
The paper also found that despite restrictions placed on the use of
DDT more than 30 years ago, concentrations of the toxin are on the rise.
Indigenous people carry an unequally high proportion of this global
toxic burden. For instance, according to Environment Canada’s National
Pollutant Release Inventory (NPRI) there are 212 Indigenous
communities in Canada living near or downstream from pulp mills and
other facilities that produce dioxins and furans.
One striking example is the old Dryden pulp mill near Grassy Narrows
which, according to the Grassy Narrows and Islington Bands Mercury
Disability Board, dumped tonnes of dioxin-laced mercury wastewater
into the English-Wabigoon River system from 1962-70. Forty years
later, the poisonous waste continues to pose a “serious health threat”
to Grassy Narrows and the Wabaseemoong First Nations, says the
Disability Board. No formal steps have been taken toward remediation
by federal or provincial governments.
The Tohono O’odham Nation’s experience bears a close resemblance to
Grassy Narrows: the world’s highest rate of diabetes can be found in
the southwest Arizona nation. According to Tribal health officials,
nearly 70 per cent of the population of 28,000 has been diagnosed with
the illness. The O’odham People make up the second largest Indigenous
Nation in the United States.
Lori Riddle is a member of Aquimel O’odham Community and founder of
the Gila River Alliance for a Clean Environment (GRACE).
GRACE was instrumental in the 10 year struggle against a hazardous
waste recycling plant that operated without full permits on O’odham
land for decades. Owned by Romic Environmental Technologies
Corporation, the plant continuously spewed effluents into the air
until it was finally shut down in 2007.
The Romic plant was not the first contributor to the O’odham’s toxic
burden, explained Riddle. Looking back to her childhood, she recalled:
“For nearly a year, [when] a plane would go over our heads, you could
see the mist. We never thought to cover our water. The chemicals just
took over and they became a part of us.”
>From the early 1950s until the late 60s, cotton farmers in the Gila
River watershed routinely sprayed DDT onto their crops to protect them
from bollworms. According to the Agency of Toxic Substances and
Disease Registry (ATSDR), each and every year, the farmers used
roughly Twenty-three pounds of DDT per acre.
In 1969, the State of Arizona banned the use of DDT; by this time the
river was gravely contaminated. According to the ATSDR, farmers then
switched to Toxaphene, a substitute for DDT—until it was banned by the
US government in 1990.
Because of these chemicals, Riddle explains, the O’odham were forced
to abandon their traditional foods and adopt a western diet. Farms
also went into a recession, forcing many families to leave their
communities. Companies, such as Romic, began moving on to their
territory, exasperating the situation. “It’s taken a toll on our
quality of life,” she says. “I’ve cried myself to sleep.”
The O’odham are dealing with what Riddle terms “cluster symptoms”
including miscarriages, arthritis in the spine, breathing problems,
unexplainable skin rashes, and problems regenerating blood cells. This
in addition to diabetes, which frequently leads to renal failure,
blindness, heart disease, and amputations.
More and more studies are being published that show the link between
diabetes and persistent organic pollutants like DDT—stemming from the
landmark “Ranch Hand” study. In 1998, the study found a 166 per cent
increase in diabetes (requiring insulin control) in US Air Force
personnel who were sprayed with the herbicide and defoliant Agent
Orange during the Vietnam War. The study also found that as dioxin
levels increased so did the presence and severity of Type 2 diabetes,
the time to onset declined following a similar trend.
However, Dr. Carpenter notes that because of the widely-endorsed
belief that diabetes is a life-style disease related to diet and
exercise, the link is gaining little attention by governments, news
agencies, or by any of the hundreds of non-profit diabetes foundations
around the world. “[It] hasn’t even made it into the medical community
at this point,” Dr. Carpenter adds. “It takes a long time to change
both medical and public opinion.”
“Clearly one thing everyone can do is to eat less animal fats,”
suggests Dr. Carpenter. Several Indigenous communities in northern
Manitoba and British Columbia have begun to do this, planting their
own gardens and building greenhouses; returning, in a traditional
sense, to some of the foods that sustained them for millennia. Others
are turning to exercise, which plays a vital role not just in the
prevention of diabetes, but in their overall health.
“Also, we must find ways of getting the POPs out of the animals that
we eat. That is not going to be easy, given how contaminated we have
made the world,” adds Dr. Carpenter. For this, Lori Riddle, who is
herself a diabetic, points to the Tribal Council and the Federal
Government.
John Schertow is an Indigenous rights advocate and author of the blog,
Intercontinental Cry.
Additional Resources
Videos
Introduction to Persistent Organic Pollutants
Introduction to PCBs
Plastics and Marine Debris in the world’s oceans
Film: The Gift of Diabetes
Studies
Three Patterns of Rising type 2 Diabetes Prevalence in the World
Pesticide Exposure and Self-Reported Gestational Diabetes Mellitus
Epidemiology of diabetes mellitus among First Nations and non-First
Nations adults
POPs lead to insulin resistance in rats
An Exploratory Study of Diabetes in a First Nation Community with
Respect to Serum Concentrations of p,p’-DDE and PCBs and Fish Consumption
Association Between Insulin Resistance and Co-Exposure to Dioxins and
Mercury
Temporal changes in PCB and DDE levels among a cohort of frequent and
infrequent consumers of Great Lakes sportfish
Reports
New Research: Nitrates and Nitrites May Cause Alzheimer’s, Diabetes
and Parkinson’s Disease
Environmental toxins, a potential risk factor for diabetes among
Canadian Aboriginals
Inorganic mercury causes pancreatic beta-cell death
Pollution Linked To Obesity, New Study Finds
Persistant Organic Pollutants may be the cause of diabetes epidemic
NOT obesity
Long-term Pesticide Exposure May Increase Risk of Diabetes
Common Herbicides and Fibrates Block Nutrient-Sensing Receptor Found
in Gut and Pancreas
Tasmania: Chronic diseases and chemical exposure. The Burden of Diabetes
BPA Linked to Heart Disease, Diabetes
Confronting Chronic Pollution: A Socio-Legal Analysis of Risk and
Precaution
Mother Load: Arsenic May Contribute to Gestational Diabetes
Report: Strong Correlation Between Diabetes and Air Pollution
Higher farmworker risks include diabetes, respiratory disease
Further Reading
Toxic shock: Does dioxin trigger diabetes
Environmental pollution and diabetes: a neglected association
DDT used as a chemical warfare agent on Indigenous People
Diabetes hits almost half of aboriginal women
Manitoba diabetic refused insulin for living on reserve
Inside the DDT Propaganda Machine
Thanks to John Hummel for his tireless research efforts
Pollution and Diabetes
Source: Emerging Health Threats Forum
About the Emerging Health Threats Forum:
http://www.eht-forum.org/common/aboutus.html
Friday 29 January 2010
Beyond diet in diabetes
Pollutants interact with obesity to raise diabetes risk
Exposure to dioxins is linked to insulin resistance, which causes
diabetes, according to research published this month in Epidemiology.1
Experts say that there is now strong evidence for a link between
diabetes and exposure to persistent organic pollutants (POPs),
including dioxins, but that this is still being largely overlooked by
the medical community.
“There’s just been a flood of evidence linking POPs to diabetics in
the last five years,” says David Carpenter, Director of the Institute
for Health and the Environment at the University at Albany, New York,
USA. “When you put this study in the context of what’s being done in
other groups, it gives a very convincing story.”
The researchers, led by Jung-Wei Chang of the National Cheng Kung
University in Tainan, Taiwan, measured the levels of serum dioxins,
fasting glucose, and insulin in 1234 people living near an abandoned
pentachlorophenol manufacturing plant. They used a homeostasis model,
which uses fasting glucose and insulin levels to estimate insulin
resistance. After controlling for risk factors such as age, obesity,
and family history of diabetes, they found a positive association,
with a linear dose-response, between serum dioxins and the prevalence
of insulin resistance.
Earlier studies have linked a variety of POPs, including dioxins,
polychlorinated biphenols (PCBs) and organochlorine pesticides such as
DDT, to an increased risk of type II diabetes. Since obesity is linked
with greater levels of POPs in the body, scientists speculate that the
link between obesity and the development of diabetes might be mediated
through these toxins.
“People get obese because they eat too much animal fat, and that’s
where the contaminants are,” Carpenter points out. This effect may
explain why indigenous populations in Canada are at higher risk of
diabetes, Carpenter explains, as they are often exposed to greater
levels of POPs than the general population.
One study in particular,2 led by Duk-Hee Lee of the Kyungpook National
University in Daegu, Korea, looked at 2016 participants to the
1999–2002 National Health and Nutrition Examination Survey, which took
blood samples from a cross section of the general US population, and
found no association between obesity and diabetes among people with no
detectable levels of POPs in their blood. This implies that the risk
of diabetes from obesity could be largely due to POPs, which
accumulate in adipose tissue, rather than physiological changes that
come with obesity, Carpenter says.
“I am somewhat sceptical of that finding,” says David Jacobs,
Professor of Public Health at the University of Minnesota and one of
Lee’s co-authors. The association between exposure to POPs and
diabetes is stronger in obese people, he points out. But it’s clear
that POPs and obesity interact to raise the risk of diabetes, he says.
This would suggest that losing weight may only partially reduce the
risk for diabetes. POPs accumulate in adipose tissue — which means
that weight loss releases the toxins back into the blood. “That stuff
has got to go somewhere,” Jacobs says. “It’s clear that POPs [released
from fat deposits] distribute into blood and other tissues.”
Worryingly, some data show a stronger association with diabetes at low
concentrations of POPs, Jacobs says. “We have seen that kind of
pattern, but it’s very difficult to interpret,” says Jacobs. Because
of the difficulty of measuring low-level exposure to these pollutants,
a lot more research is needed to confirm whether they have this
effect, he argues.
Despite the body of evidence linking POPs and diabetes, the link is
still not widely acknowledged in the medical community. “Physicians
are totally oblivious to this being a risk factor,” Carpenter says.
“The nutrition community have oversold the benefits of fish and
underplayed the dangers of contaminants.”
Although production of many of the toxins studied has been banned
worldwide, they persist in the environment, are distributed globally,
and continue to bioaccumulate in the food chain. Pesticides like DDT,
which are still used in malarial regions, can turn up in the food
supply all over the world. And others are still on the increase.
“[POP] exposure is to some degree going down, except in the case of
flame retardants where exposure is increasing exponentially,”
Carpenter says. Flame retardants are structurally very similar to
PCBs, he points out, and so these too should be investigated for the
potential to cause diabetes — especially as children are among the
most highly exposed population groups.
Reference and links
1. Chang JW, Chen HS, Su HJ, Liao PC, Guo HR,and Lee CC. Dioxin
Exposure and Insulin Resistance in Taiwanese Living Near a Highly
Contaminated Area. Epidemiology 2010;21:56–61.
doi:10.1097/EDE.0b013e3181c2fc6e
2. Lee DH, Lee IK, Song K, Steffes M, Toscano W, Baker BA and Jacobs
JR. A Strong Dose-Response Relation Between Serum Concentrations of
Persistent Organic Pollutants and Diabetes. Diabetes Care
2006;29:1638–1644. doi:10.2337/dc06-0543
Epidemiology:
January 2010 - Volume 21 - Issue 1 - pp 56-61
doi: 10.1097/EDE.0b013e3181c2fc6e
Endocrine: Original Article
Dioxin Exposure and Insulin Resistance in Taiwanese Living Near a
Highly Contaminated Area
Chang, Jung-Wei; Chen, Hsiu-Ling; Su, Huey-Jen; Liao, Po-Chi; Guo,
How-Ran; Lee, Ching-Chang
Abstract
Background: Several epidemiologic studies suggest a slightly increased
risk of type 2 diabetes in relation to background levels of dioxins.
Little is known about how serum dioxins might affect insulin
resistance, a hallmark of type 2 diabetes. We examined the association
between exposure to dioxins and insulin resistance.
Methods: We investigated 1234 nondiabetic persons living near a
deserted pentachlorophenol factory. Using high-resolution gas
chromatography/high-resolution mass spectrometry and blood
biochemistry tests, we measured serum dioxins, fasting glucose, and
insulin. Finally, we examined associations between serum dioxin levels
and the homoeostasis model assessments of insulin resistance and
pancreatic β-cell function.
Results: Participants with insulin resistance (index at or above the
75th percentile) had higher dioxin levels (24.3 vs. 19.8 pg
WHO98-TEQDF/g lipid) than those without insulin resistance. In both
the crude and adjusted models, insulin resistance increased with serum
polychlorinated dibenzo-p-dioxins and dibenzofuran (PCDD/F) levels. We
found a slight monotonic increase in insulin resistance across the
serum PCDD/F categories (P for the trend <0.001). Groups with serum
dioxin levels higher than 20.5 pg WHO98-TEQDF/g lipid had higher
insulin resistance (adjusted odds ratios of 2.7, 3.5, and 5.0 for 50th
to <75th, 75th to <90th, and ≥90th percentile, respectively) compared
with the reference group (<9.6 pg WHO98-TEQDF/g lipid [< 10th
percentile]).
Conclusions: After adjusting for confounding factors, we found a
positive association between serum dioxins and the prevalence of
insulin resistance.
News Release Re: Pollution and Diabetes
Dear Friends,
The pollution/diabetes connection has received no major news coverage
anywhere in the world. I hope you will share the media release below
with all your media contacts. Also, please share this information with
all your scientific, environmental and Tribal colleagues who are
studying diabetes. Much is at stake for the health of people all over
the world. All the very best to you.
For Land and Life,
John H.W. Hummel,
Volunteer Pollution/Health Researcher,
611 Eighth Street, Nelson B.C.
Canada
(250)505-2165
Email: jhwhummel at shaw.ca
Story Idea: The Link between Pollution and Diabetes
Health Canada Predicts that within 10 years, 27% of all First Nations
people in Canada will have Type II Diabetes. Many First Nations People
have been exposed to toxins such as DDT, Dioxin, Arsenic, Cadmium
Hexachlorobenzene and PCB's for many decades.
For a Summary of the latest Scientific research on this topic, please
go to:
http://www.ajmed.fr/documents/pdf/perturbateurs_diabete.pdf
For some of the very latest studies on pollution/diabetes links please
go to:
http://groups.google.ca/group/friends-of-agg/browse_thread/thread/6cb3503501
b8b59c?hl=en
(and click on 'show quoted text')
The Pesticide DDT, Persistant Pollutants and Diabetes:
http://groups.google.com/group/friends-of-agg/browse_thread/thread/13b91035f
72b2ce9
Key Scientific Contacts Re: Diabetes and Pollution
(Please Note, above are links to many of these scientists most
recently published and peer reviewed studies on the pollution/diabetes
connections):
1) Dr. David Carpenter carpent at uamail.albany.edu United States
2) Dr. Duk-Hee Lee lee_dh at knu.ac.kr Korea
3) Dr. Joel Michalek michalekj at uthscsa.edu United States
4) Dr. Mary Turyk mturyk1 at uic.edu United States
5) Dr. Miquel Porta mporta at imim.es Spain
6) Dr. Lars Rylander lars.rylander at med.lu.se Sweden
7) Dr. Anna Rignell-Hydbom anna.rignell-hydbom at med.lu.se Sweden
8) Dr. Laurie Chan lchan at unbc.ca Canada
9) Dr. Harold Schwartz harold_schwartz at hc-sc.gc.ca Canada
10) Dr. Allen E. Silverstone silversa at upstate.edu United States
11) Dr. Donna Mergler mergler.donna at upstate.edu Canada
12) Dr. Jung-Wei Chang s7892102 at mail.ncku.edu.tw Taiwan
11) Dr. Donna Mergler mergler.donna at uqam.ca Canada
First Nations Pollution/Health Contacts:
Research Tools and Contacts for the Communities Re: Pollution and Health
Dear Friends,
Many communities are experiencing health problems related to exposure
to industrial pollutants. Many people want to investigate the
pollution/health links in their community but have little funding and
aren't sure where to begin. To assist people in their pollution/health
research, here are a few inexpensive community action tools to get
started and some key contacts to compare notes with and get advice
from. Hope this information is helpful to protect the health and well
being of your community. Also, here are the tools to start a broad
based coalition to eliminate pollution and protect the health of the
people and the earth. All the best to you all.
For Land and life,
Your Friend,
John H.W. Hummel
Nelson, B.C.
'Bucket Brigade' :An Inexpensive Way to Find Out What Pollution is in
Your Communities Air:
http://www.bucketbrigade.net/article.php?list=type&type=9
Body Mapping for Pollution Related Health Problems:
http://www.ohcow.on.ca/clinics/sarnia/docs/IJOEH_Holmes.pdf
More on Body Mapping: http://newsreel.org/transcripts/beloved.htm
Bucket Brigade Contacts: Denny Larson, Global Community Monitor:
denny at gcmonitor.org
Ruth Breech, Global Community Monitor: ruth at gcmonitor.org
Body Mapping Contacts: Ada Lockridge, Aamjiwnaang First Nation:
ada_lockridge at hotmail.com
James Brophy, Scientist and expert in Worker Health and safety:
jimbrophy at sympatico.ca
Here are a few key contacts for you if you wish to investigate the
health impacts of industrial pollution on First Nations, Metis and
Inuit people in North America in 2009.
1) Dr. David Carpenter,Toxicologist, University of Albany, NY:
carpent at uamail.albany.edu
- David has been doing toxics research with the Mohawks of Akwesasne
for many years and recently published scientific papers showing a
dramatic increase in Diabetes and Heart Disease in Akwesasne Mohawks
with PCB's and Pesticides in their blood
2) Henry Lickers, Akwesasne Mohawk Nation, Cornwall, Ontario:
hlickers at akwesasne.ca
- Henry has worked at the Akwesasne Environment department for decades
and can describe the impacts of PCB's, mercury, pesticides, fluoride
etc on his people
3) Ken Jock, Akwesasne Mohawk Nation, Cornwall, Ontario :
ken_jock at srmtenv.org
- Ken works on environmental issues at Akwesasne and can describe the
health impacts pollution has had on his people
4) Joyce King, Haudenosaune Environmental Task Force:
joyceking at westelcom.com
- Joyce can describe pollution/health impacts on the Six Nations
people as a whole
5) Eva Johnson, Environmental Department, Kahnawake Mohawk Nation:
(450) 635-3035 or (450) 635-0600
-Eva can describe how toxic dumpsites, Lead pollution and solvent
pollution from Industry has harmed the health of Kahnawake people e.g.
the Scleroderma, heart disease, diabetes and cancer epidemics
6) Lynn Jacobs, Environmental Department, Kahnawake Mohawk Nation:
lynn.jacobs at mck.ca
- Lynn and Eva are a team and she can well describe pollution/health
impacts in her community
7) Sue Chiblow, Chiefs of Ontario, Environmental Department: sue at coo.org
- Sue Can describe pollution/health impacts on aboriginal communities
all over Ontario
8) Dr. Michael Gilbertson, Research Scientist:
michael.gilbertson23 at gmail.com - Michael discovered possible mercury
poisoning (Minamata Disease) outbreaks at specific pollution Hotspots
around the Great Lakes and is presently assisting Aamjiwnaang First
Nation expose pollution/health problems in their area e.g. skewed
birth ratios likely attributable to pollution exposure
9) James Brophy, Research Scientist: jimbrophy at sympatico.ca
- James Co-Authored Pollution/Health papers with Michael Gilbertson
and is presently helping Aamjiwnaang First Nation expose pollution
related health problems in their community
10) Ron Plain, Aamjiwnaang First Nation, Sarnia, Ontario:
rplain at environmentaldefence.ca
- Ron is a Pollution/Health Activist at Aamjiwnaang and works at
Environmental Defence Canada to expose pollution/health issues in
Aboriginal Communities
11) Ada Lockridge, Aamjiwnaang First Nation, Sarnia, Ontario:
ada_lockridge at hotmail.com
- Heads up the Aamjiwnaang Environment Committee exposing Benzene,
Mercury etc. impacts on the health of her people
12) Wilson Plain, Aamjiwnaang First Nation, Sarnia, Ontario:
wilsonplain2 at hotmail.com
-Wilson is part of the Aamjiwnaang Environment Committee and was
recently found to have PCB's and all kinds of other industrial toxins
in his body
13) Judy DaSilva, Grassy Narrows First Nation, Ontario: jsilva at northone.ca
-Judy is a Clan Mother, Healer, environmental activist and
spokesperson at Grassy Narrows and can tell you about the mercury
poisoning in her community, the dioxins and furans found in Grassy's
wild meat and the herbicide spraying of Grassy's traditional territory
14) Steve Fobister Sr., Grassy Narrows First Nation, Ontario:
gsfobister at hotmail.com
- Steve is a Councillor at Grassy Narrows First Nation and has been a
leader of his people for decades.
Steve can tell you about what has happened at Grassy from all the
pulp-mill pollution and herbicide spraying.
My pal Steve, his daughter and his little Granddaughter and many of
his other family members all have Mercury Poisoning from that Pulp
Mill at Dryden
15) Joe B. Fobister, Grassy Narrows First Nation, Ontario:
jbfobister at yahoo.ca
- Joe is a spokesperson for the Grassy Blockaders and a leader of his
community. He can tell you all about what the pollution has done to
the health of his people
16) Sherry Fobister, Grassy Narrows First Nation, Ontario:
namesfobister at hotmail.com
-Sherry is another dear friend. She is a great spokesperson and can
tell you firsthand about the difficulties she has faced as a single
Mum dealing with her own mercury related health problems as well as
that of her little daughter Catherine
17) Emily Fobister, Grassy Narrows First Nation,Ontario:
mommie52006 at hotmail.com
- Emily did a Sacred walk to help her people heal from all the
industrial sicknesses harming her family and people. She inspired many
youth and helped many people.
18) Dr. Masazumi Harada, Mercury Expert in Japan: mharada at kumagaku.ac.jp
- Dr. Harada discovered mercury poisoning at Grassy Narrows and
Whitedog in the 1970's and found new cases amongst Grassy children
when he returned and tested people in 2003.
19) Dr. Leanne Simpson, Expert on First Nations Pollution/Health
Issues: leannesimpson at sympatico.ca
- Leanne worked on the Grassy Narrows/Wabauskang wild meat testing
study and is presently investigating all the deaths and sickness among
Wabauskang people from when they lived at Quibel, Ontario immediately
downstream from the Dryden Pulp Mill
20) Betty Riffel, Wabauskang First Nation, Ontario: bet093 at hotmail.com
- Betty is working with Leanne Simpson to investigate the deaths of
all those infants when her people lived at Quibel. She also worked on
the Grassy Narrows/Wabauskang wild meat study where they recently
found mercury, furans etc. in the fish and wildmeat eaten by the people
21) Damien Lee, Fort William First Nation, Ontario:
connectwithdamien at gmail.com
-Damien heads up the Anishinabek of the Gitchi Gami (AGG)
environmental group at Fort William First Nation and is knowledgable
about the hundreds of random dumpsites at his community, the pollution
from local industry surrounding his community and much more!
22) Wendy Solomon, Fort William First Nation, Ontario:
ladysigni_sha at msn.com
- Wendy is the outreach coordinator for AGG and another dedicated
environmental/health advocate at Fort William First Nation who knows
alot about pollution/health issues
33) Betsy Mandamin, Grand Council Treaty 3, Kenora, Ontario:
health at treaty3.ca
- Betsy works at Treaty 3 Health department and has much knowledge of
Mercury pollution and environmental/health issues in the whole Treaty
3 Area
34) Dorothy Friday, Grand Council Treaty 3, Kenora, Ontario:
health at treaty3.ca
- Dorothy also works at Treaty 3 Health Department and knows alot
about pollution/health issues in the Treaty 3 Area
35) Steve and Susanne Lawson, First Nations Environment Network
(FNEN), Tofino, B.C.: councilfire at hotmail.com
- Steve and Susanne co-ordinate FNEN, are lifelong environmental
activists and can put you in touch with dozens of Aboriginal
communities impacted by pollution
36) Tom Goldtooth, Director, Indigenous Environment Network (IEN):
ien at igc.org
- Tom Coordinates the IEN south of the border, a big focus of IEN has
been pollution/health issues and he can put you in touch with
Aboriginal communities who have health problems due to pollution all
over North America and beyond!
38) Allister Marshall, FNEN - East Coast: amarshall at potlotek.ca
-Allister is very knowledgable about pollution/health issues impacting
First Nations on the East Coast of Canada
39) Ishbel Munro, FNEN - East Coast: coastalnet at ns.sympatico.ca
-Ishbel has been an advocate for environmental/Aboriginal issues for
decades and can put you in touch with pollution impacted First Nations
all over (especially in Nova Scotia)
40) Willi Nolan, Elder/Environmental Activist, East Coast: willi at web.ca
- Willi is a respected Anishinawbe Elder who is very knowledgable
about pollution/health impacts on First Nations communities. Willi's
main focus is to share traditional knowledge of the environment and
Mother Earth with the youth. Willi has done truly remarkable things!
Someone should write a book about her.
41) Al Hunter, FNEN - Ontario: tbird2 at netscape.net
- Al Hunter is a former Chief of his people, a respected Elder (even
though he is young) and knows lots about pollution in the Manitou
Rapids, Rainy River area of Ontario. He has many contacts knowledgable
about pollution/health impacts on Aboriginal communities.
42) Fred Greene, Grand Council Treaty 3, Kenora, Ontario:
fred.greene at treaty3.ca
- Fred is a political advisor to the Ogichida of Grand Council Treaty
3 and is very knowledgable about pollution impacts on the Treaty 3
First Nations
43) Alan Penn, Expert on Mercury Poisoning of James Bay Cree: apenn at gc.ca
- Alan is an expert on the Mercury pollution of the James Bay Cree
communities
44) Jennifer Foulds, Environmental Defence Canada (EDC):
jfoulds at environmentaldefence.ca
- Jennifer works with Ron Plain at EDC. EDC is presently engaged in
uniting First Nations, Environmental NGO's and Scientists to battle
pollution impacting the health of us all.
45) David McLaren, Saugeen First Nation, Ontario: d.mclaren at the-matrix.ca
- David is a pollution/health/environment expert from Saugeen First
Nation
46) Dean Jacobs, Walpole Island First Nation, Ontario:
dean.jacobs at wifn.org
- Dean is a pollution/health/environment expert at Walpole Island
First Nation
47) Dr. John O'Connor, Former Dr. for Fort Chipewyan People:
gramocroi at shaw.ca
- Dr. O'Connor discovered rare cancers in the people of Fort Chipewyan
First Nation in Alberta likely due to pollution from Tar sands
development. The Government has been hounding him and trying to take
away his Physicians lisence ever since he went public with his
concerns for Fort Chipewyan people.
48) George Poitras, Health Official, Fort Chipewyan Area:
george.poitras at shawbiz.ca
- George is one of the spokespeople for First Nations in Alberta
concerned about pollution/health problems associated with Tar sands
Development in northern Alberta.
49) Kevin Timoney, Researcher: ktimoney at compusmart.ab.ca
- Kevin did a huge report on pollution from the Tar Sands development
which could be harmful to First Nations in the area.
50) Winona LaDuke, Famous First Nations Environmental Activist:
honorearth at earthlink.net
-Winona is a very famous Native American environmental activist who
can tell you alot about pollutions health impacts on Aboriginal
communities all over North America
51) Chief Thomas Alexis, Chief of Tl'azt'en First Nation, B.C.:
thomas.alexis at tlazten.bc.ca
- Many of Chief Alexis's people are sick and dying of mercury
poisoning from an old mercury mine in northern B.C. He has many
stories to tell on that topic.
52) Brenda Duncan, Haisla First Nation, Kitimat, B.C.:
executivedir at uniserve.com
- Brenda heads up the Nanakila Institute which protects the
environment in Haisla Traditional Territory. She can tell you about
the impacts of pollution from Alcan, Eurocan and Methanex on the
health of her people
53) Sheila Watt-Cloutier, Famous Inuit Leader and Environmental
Activist: iccan at baffin.ca
- Sheila is a very famous Inuit leader and environmental activist who
can tell you all about what the mercury, dioxin and PCB's from
Southern industry has done to the health of Aboriginal people of the
Circumpolar Region
54) Ramsey Hart, Mining Watch Canada: ramsey at miningwatch.ca
- Ramsey heads up Mining Watch Canada which is a collaberation of
environmental NGO's, First Nations organizations and labour groups. He
can tell you lots about the impacts of mining and smelting impacts on
the health and well being of aboriginal communities all over Canada.
55) Jamie Kneen, Mining Watch, Canada: jamie at miningwatch.ca
- Jamie is an aboriginal rights/environmental justice activist from
way back! He is a treasure trove of knowledge and contacts on
pollution impacts in Aboriginal communities.
Aboriginal Women Suffer Surge in Diabetes
Link to full text of New Study:
http://www.cmaj.ca/cgi/rapidpdf/cmaj.090846v1
Link to Article on Gestational Diabetes and Pesticide Exposure:
http://www.environmentalhealthnews.org/newscience/2007/2007-0706saldanaetal.
html
Link to Full Text of Gestational Diabetes/Pesticide Exposure Study:
http://care.diabetesjournals.org/content/30/3/529.full
Please Note: Pesticides have been found in the fish and wildmeat eaten
by many First Nations communities all across Canada. That is in
addition to the body burden of pesticides we all carry by simply
eating a variety of store bought foods.
Aboriginal women suffer surge in diabetes
Native people, especially women, are developing the disease in their
40s – 30 years sooner than non-natives, study finds
André Picard Public Health Reporter
>From Tuesday's Globe and Mail Published on Tuesday, Jan. 19, 2010
9:16AM EST Last updated on Tuesday, Jan. 19, 2010 9:45AM EST
The rate of diabetes among aboriginal women is four times that of
women in the general Canadian population, a new study reveals.
Moreover, members of first nations are developing the debilitating
illness by their 40s, while in the rest of society it tends to strike
people in their 70s.
“Diabetes is a disease of young first-nations adults with a marked
predilection for women,” said lead author Roland Dyck of the
department of community health and epidemiology at the University of
Saskatchewan.
“In contrast, diabetes is a disease of aging non-first-nations adults
that is more common in men,” he said.
Dr. Dyck said the big difference in the age of onset has serious
implications; diabetes is one of the principal causes of blindness,
amputations, kidney failure and heart disease.
The study, published in the Canadian Medical Association Journal,
examined trends among patients diagnosed with diabetes in Saskatchewan
from 1980 to 2005. The sample included 8,275 aboriginal people and
82,306 non-aboriginals.
The data paint a troubling picture of an unrelenting diabetes epidemic
in native communities that “is likely to continue increasing in the
foreseeable future,” the paper notes.
Dr. Dyck and his team found that in 2005, 20 per cent of women and 16
per cent of men living in native communities had Type 2 diabetes. That
was up sharply from 9.5 per cent and 4.9 per cent respectively in 1980.
Rates of diabetes in the non-aboriginal population rose to 5.5 per
cent from 2 per cent in women over the same period, and to 6.2 per
cent from 2 per cent in men.
Over all, the incidence (the frequency of development of diabetes in a
population over a given time period) and the prevalence (the number of
people currently suffering from the disease) were both about four
times higher among aboriginal women and 2.5 times higher among
aboriginal men.
The epidemiological study was not designed to explain the underlying
causes of this disparity, but Dr. Dyck put forth a couple of likely
explanations.
First, it has been well documented that rates of overweight and
obesity are significantly higher in native communities. (Excess
weight, particularly in the abdominal area, is a key factor in Type 2
diabetes.) In aboriginal communities, women are more likely to be
overweight or obese than men, and at a younger age.
Second, there are high rates of gestational diabetes in pregnant
aboriginal women. Those who develop diabetes during pregnancy are at
high risk of developing Type 2 diabetes later in life, and so are
their children.
“Gestational diabetes has been implicated in the intergenerational
‘vicious cycle’ by increasing diabetes among the offspring,” Dr. Dyck
said.
He added that the differences in the epidemiology of the disease in
native and non-native people means prevention programs should be
different as well.
In particular, programs for first nations should focus on women in
their reproductive years and on preventing gestational diabetes, Dr.
Dyck said.
There are three distinct forms of diabetes: Gestational diabetes is a
temporary condition that occurs during pregnancy; Type 1 diabetes,
usually diagnosed in children, occurs when the pancreas is unable to
produce insulin; Type 2 diabetes occurs when the pancreas does not
produce enough insulin, or the body does not effectively use the
insulin it produces.
About 90 per cent of diabetics have Type 2 disease, which is usually a
consequence of obesity, inactivity, poor diet and aging. Poverty is
also strongly associated with diabetes, which could be another factor
that helps explain high rates in native communities.
Dear Friends,
The discovery, in the new scientific study described below, is very
significant regarding the relationship between exposure to persistent
organic pollutants and the onset of insulin resistance related
diseases like Type II Diabetes. You can view the full text of this
important study at this Link:
http://ehp.niehs.nih.gov/members/2009/0901321/0901321.pdf
All the best to you.
For Land and Life,
John H.W. Hummel
Pollution/Health Researcher
Nelson, B.C.
Canada
Environmental Health News - January 14, 2010
POPs lead to insulin resistance in rats.
Jan 14, 2010
Ruzzin J, R Petersen, E Meugnier, L Madsen, EJ Lock, H Lillefosse, T
Ma, S Pesenti, SB Sonne, TT Marstrand, MK Malde, ZY Du, C Chavey, L
Fajas, AK Lundebye, CL Brand, H Vidal, K Kristiansen and L Froyland.
2009. Persistent organic pollutant exposure leads to insulin
resistance syndrome. Environmental Health Perspectives
doi:10.1289/ehp.0901321.
Context
What did they do?
What did they find?
What does it mean?
Resources
More new science from EHN
----------------------------------------------------------------------------
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Synopsis by Negin P. Martin, Ph. D , Kathleen M. McCarty, Sc.D. and
Wendy Hessler
ShareThis
NatalieMaynor/flickr
Male rats fed fish oil from farmed salmon developed insulin
resistance, obesity and related health issues.
A new study in rats shows that persistent organic pollutants (POPs) –
at levels found in food – cause insulin resistance and associated
obesity and liver disease in the animals. The study is the first to
show this experimentally. Insulin resistance can lead to type 2
diabetes, which is becoming a global epidemic. The association between
high levels of POPs in people and increased chance of developing
diabetes has been known since 2006. Until now, scientists could not
positively conclude that POPs influenced the onset of diabetes.
Context
Persistent organic pollutants (POPs) are a diverse group of toxic
chemicals that resist degradation and can remain in the environment
for decades. The compounds are known to adversely affect health in
people and wildlife.
POPs include organochlorine pesticides, polychlorinated biphenyls
(PCBs), dioxins and furans. Many of the synthetic chemicals were
created for use in agriculture and construction. Others were used in,
or are byproducts of, industry. Some – such as dioxins – also occur
naturally as a result of burning and combustion.
The US and Europe banned the production and use of certain POPs more
than 30 years ago. This ban was expanded globally during this century.
Yet, due to their chemical nature, they can remain intact, persist in
the environment and accumulate in wildlife and people. They build up
in farmland soils and waterways, contaminating wildlife and making
their way up the food chain. People are exposed through eating
contaminated fish, poultry, meat and dairy products.
The hormone insulin helps in the uptake and storage of the sugar
glucose – a basic regulator of metabolism. Insulin resistence occurs
when cells do not respond to the hormone. This allows glucose levels
to build up in the blood and leads to more serious health problems.
Additionally, insulin and the uptake of glucose regulate the formation
of fat.
In the U.S., one out of four adults have metabolic abnormalities that
are associated with insulin resistance. Typical symptoms of insulin
resistance are fatigue, obesity, accumulation of fat around the belly
and difficulty regulating the blood levels of fat and sugar. Insulin
resistance is the underlying cause of type 2 diabetes, cardiovascular
problems and liver disease.
These drastic increases in metabolic disorders cannot be totally
explained by current known risk factors – high fat diets and lack of
exercise. Based on animal and human research findings, some scientists
suspect that POPs have the potential to contribute to the diabetes
epidemic that threatens people around the globe. Human studies have
found associations between an increased chance of developing type 2
diabetes and higher levels of POPs in the body (Lee et al. 2006).
Animal research has pointed in the same direction.
What did they do?
Adult male rats were fed for 28 days either crude or refined fish oil
obtained from farmed Atlantic salmon carcasses.
The crude fish oil contained the levels of POPs that people are
typically exposed to after eating the fish. The refined fish oil
contained no POPs and was fed to the control rats. The levels of fat
in both diets were the same.
After exposure, the researchers measured body weight, whole-body
insulin sensitivity and levels of POPs in each group. They compared
the levels of fat, triacylglycerol, diacylglycerol and cholesterol in
the rat livers.
They also determined how well rats could regulate sugars and fats and
measured the expression of several key genes that are thought to be
involved in the metabolic process.
In a parallel study, fat cells were exposed to the types of POPs that
were stored in the fish fat cells at similar levels found in the
salmon oil. The effects on sugar uptake by the cells were measured.
What did they find?
Adult rats exposed to the crude fish oil – which contained the POPs
mixture – put on belly fat and developed insulin resistance and liver
disease. The rats could not regulate fat properly. They had higher
levels of cholesterol and the fatty acids triacylglycerol and
diacylglycerol in their livers.
In contrast, none of these changes were seen in the rats that ate fish
oil without the POPs.
Although blood levels of insulin and sugar were similar among rats
with either diet, the rats exposed to POPs had impaired insulin
action. The POPs also altered the expression of number of genes
involved in metabolism, which could explain the changes in fat and
sugar regulation.
Similar results on insulin and gene expression were seen in the
cultured fat cells that were exposed to a POPs mixture similar to that
found in the fish oil. The POPs – especially the organochlorine
pesticides – drastically inhibited insulin's action and the cells'
ability to take up glucose, a first step in insulin resistence.The
cells expressed fewer of the genes that regulate fat and sugar levels.
Further analysis showed the liver and fat tissue differed in the
components they predominantly store. PCBs and organochlorine
pesticides were measured in both liver and fat tissue while certain
types of dioxins and furans were more abundant in the liver.
What does it mean?
Based on this study, daily exposure to POPs mixtures in food at levels
found naturally in the environment leads to insulin resistance and an
impaired ability to metabolize fat and sugar in adult male rats. The
levels measured in the rats' fat tissues were relevant to humans, as
they were similar to those previously reported for middle-aged Europeans.
This rodent study is the first to find that POPs can cause abnormal
insulin action and adds an important missing piece to the growing body
of human research that has found associations between POPs levels and
insulin resistance that could cause such serious health problems as
type 2 diabetes, obesity and liver disease.
Generally, animal studies provide a way to ask and answer
health-related questions that cannot be studied directly in people.
Humans and rats share similar hormones that work in the same general
way to guide metabolism and reproduction. Because of these
similarities, rats and mice are used to assess both potential drug
therapies and potential effects from environmental toxicants. Results
from animal studies supply insights into what might be occurring with
respect to health and disease in people.
Animals and people accumulate these long-lived compounds from food and
store them in fat. Most of us carry at least some types of the
chemicals in our bodies. The authors say their results indicate that
POPs – as with some other indicted environmental chemicals found in
air pollution and plastics – "provide additional evidence that global
environmental pollution contributes to the epidemic of insulin
resistance-associated metabolic diseases."
The World Health Organization estimates that more than 300 million
people will die from disease associated with insulin resistance and
metabolic disorders by 2015. The current strategies for prevention
include limiting dietary intake and increasing physical activity. This
study suggests that considering the role of POPs may be warranted in
prevention strategies.
Current methods of risk assessment may also fall short in protecting
health, since different types of POPs mixtures impaired insulin action
differently. Some did, while others did not. The dioxin and
dioxin-like PCB levels that changed insulin action did not fall within
the standard measure of toxicity – called the total toxic equivalent
(TEQ) concentration – that is currently used to regulate safe
exposures to environmental chemicals. The findings "demonstrate that
risk assessment based on TEQ assigned to dioxins and dioxins-like
PCBs" does not include the risk of insulin resistance, according to
the study's authors.
POPs production and use are regulated worldwide. For example, in the
U.S., regulations imposed by the Environmental Protection Agency have
significantly reduced the release of dioxins and furans. Globally, a
number of international laws limit or ban their use.
The chemicals classified as POPs do not degrade easily, so even
limited production will still have an additive effect over the years.
Because of this, POPs will continue to impact the environment – and
possibly human health – into the future.
ShareThis
Resources
Insulin resistence and pre-diabetes. The National Diabetes Information
Clearinghouse, The National Institute of Diabetes and Digestive and
Kidney Diseases.
Lee, DH, IK Lee, K Song, M Steffes, W Toscano, BA Baker and DR Jacobs.
2006. A strong dose response relation between serum concentrations of
persistent organic pollutants and diabetes: Results from the National
Health and Examination Survey 1999-2002. Diabetes Care 29(7):1638-1644.
Persistant organic pollutants. United Nations Environment Programme.
Stockholm Convention on Persistent Organic Pollutants. Stockholm
Convention.
Contaminants and diabetes
Search
13 October Dioxin tied to metabolic syndrome in Japan. A large new
epidemiological study in Japan finds that even at background levels of
exposure, people with higher levels of dioxin and dioxin-like PCBs are
a significantly greater risk to metabolic syndrome, which includes
high blood pressure and Type 2 diabetes. Environmental Health News.
18 August In human fat tissue, Bisphenol A inhibits release of a
hormone that protects people from diabetes and heart attacks. In human
fat tissues, bisphenol A suppresses levels of a key hormone,
adiponectin, that protects people from heart attacks and Type II
diabetes. Environmental Health News.
3 May Insulin dependant diabetes mellitus: implications for male
reproductive function -- Agbaje et al., 10.1093/humrep/dem077 -- Human
Reproduction Men with diabetes have increased levels of DNA damage in
their sperm. Human Reproduction.
15 April Birth Weight and Subsequent Risk of Type 2 Diabetes: A
Meta-Analysis -- Harder et al. 165 (8): 849 -- American Journal of
Epidemiology There is a non-monotonic relationship between birth
weight and risk of Type II diabetes later in life. American Journal of
Epidemiology.
6 January Increased rate of hospitalization for diabetes and
residential proximity of hazardous waste sites. People living closer
to hazardous waste sites containing persistent organic pollutants are
more likely to be hospitalized for diabetes. Environmental Health
Perspectives.
More news about
Contaminants and diabetes
Copyright © 2003 Environmental Health Sciences. All rights reserved.
Dear Friends,
The world is in the midst of a Type II Diabetes epidemic.
In 2008 and 2009, many new studies have been published concerning
links between pollutants and the onset of Type II Diabetes. The key
study which got world scientists looking into these links in the last
several years was the one conducted by Dr. Duk-Hee Lee (full text of
that study is below). She has also published subsequent studies on
this topic. Here is a quote from Dr. Miquel Porta from the prestigious
journal 'The Lancet' regarding Dr. Lee's findings:
“Another striking finding in Lee and co-workers' study is that there
was no association between obesity and diabetes in individuals with
non-detectable levels of persistent organic pollutants. Obesity was a
risk factor for diabetes only if people had blood concentrations of
these pollutants above a certain level. This finding might imply that
virtually all the risk of diabetes conferred by obesity is
attributable to persistent organic pollutants, and that obesity is
only a vehicle for such chemicals. This possibility is shocking.”
Here also, is the full text of Dr. Porta's letter to The Lancet
regarding that important Lee study. I hope you will share this email
with anyone who has not seen it and might find it of interest for
their research. All the best to you.
For Land and Life,
John H.W. Hummel,
Pollution/Health Researcher,
611 Eighth Street,
Nelson, British Columbia,
Canada V1L 3A6
(250) 505-2165
jhwhummel at shaw.ca
The Lancet
August 12, 2006
Persistent organic pollutants and the burden of diabetes
Miquel Porta a, b, mporta at imim.es
Studies from the USA1,2 have drawn attention to the possibility that
persistent organic pollutants might contribute to cause diabetes.3-6
Dioxins, polychlorinated biphenyls, dichlorodiphenyldichloroethylene
(DDE, the main degradation product of the pesticide
dichlorodiphenyltrichloroethane [DDT]), trans-nonachlor,
hexachlorobenzene, and the hexachlorociclohexanes (including lindane)
are some of the persistent organic pollutants most commonly found in
human beings.7,8 Lipophilic and highly resistant to degradation, these
pollutants are present in many fatty foods, usually at low
concentrations.9 Because they contaminate virtually all people, even
if they confer only a low individual risk of diabetes, these
pollutants might have a substantial overall population effect.10
Dae-Hee Lee and colleagues' recent study1 is the first to analyse
serum concentrations of persistent organic pollutants and fasting
plasma-glucose concentrations in a random sample of a general
population. Previous studies have focused on selected populations,
often occupationally or accidentally exposed to high levels of such
pollutants. Not studying a less-exposed group might have led to a
blurring of risks. Widely prevalent exposures are particularly
difficult to isolate as causal agents.3 Concentrations of persistent
organic pollutants in the study are typical of levels in many
societies globally, and the risk of diabetes seems higher than ever.
After adjustment for age, sex, race, income, lipids, body-mass index,
and waist circumference, Lee and colleagues showed that the prevalence
of diabetes was more than five times higher in groups with higher
concentrations of polychlorinated biphenyl 153, oxychlordane, or
trans-nonachlor than in those with lower concentrations. The
prevalence of diabetes doubled and tripled in those in the upper
quintiles of DDE and other compounds.1
Lee and co-workers adjusted their results by multiple factors.1 Such
adjustment is fine if we wish to isolate the "pure" effect of
persistent organic pollutants on diabetes separately from that of
obesity, age, or income. However, adjustment by body-mass index and
waist circumference might be an overadjustment, because dietary fats
are the main source of persistent organic pollutants for human beings,
and the body burden of these lipophilic chemicals often increases with
increasing body-mass index. Crude or less adjusted prevalence odds
ratios would provide information about the actual prevalence of
diabetes in people with specific concentrations of these pollutants.
Indeed, a priority should be to assess the validity of the study's1
main finding: diabetes might be several times more prevalent in people
with higher concentrations of these pollutants than in those with
lower or no detectable levels. Causal inferences need to be extremely
cautious. The cross-sectional nature of Lee's study, in particular,
prompts assessment of the direction of the association: might diabetes
cause a higher accumulation of persistent organic pollutants?
Unfortunately, data for the toxicokinetics of these pollutants in
patients with diabetes are scarce, while many studies indicate that
most persistent organic pollutants are resistant to active
metabolism.1,7,8 Even if diabetes is some day shown to be the first
major disease favouring accumulation of persistent organic pollutants,
patients and clinicians would need to cope with the consequences:
individuals with diabetes would be more likely to experience the
adverse effects of these pollutants.6
Another striking finding in Lee and co-workers' study is that there
was no association between obesity and diabetes in individuals with
non-detectable levels of persistent organic pollutants. Obesity was a
risk factor for diabetes only if people had blood concentrations of
these pollutants above a certain level. This finding might imply that
virtually all the risk of diabetes conferred by obesity is
attributable to persistent organic pollutants, and that obesity is
only a vehicle for such chemicals. This possibility is shocking.
Standard measures were used for body-mass index, but weight changes
were not considered. Weight gains and weight losses in individuals
with and without diabetes will be difficult to measure in large
studies. But cohort studies with repeated measurements of individual
weight and blood could help solve the puzzle.
An association between diabetes and blood concentrations of
polychlorinated biphenyls has also been reported in a study from
Michigan.2 Although the study was prospective, diabetes was
self-assessed and participants had had accidental food contamination
30 years previously. Women in groups with higher serum concentrations
of polychlorinated biphenyls had a twofold increased incidence of
diabetes (again adjusted by several factors, including age and
body-mass index). The crude incidence also doubled in men with the
highest levels of polychlorinated biphenyls, but adjusted results were
non-significant.
Exposure to many persistent organic pollutants has fluctuated in the
past 60 years: birth cohort and period effects are plausible. But
time-series and age-period cohort analyses of the potential link
between persistent organic pollutants and diabetes are not available.
Ecological and individual-based studies would allow estimations to be
made of the fraction of diabetes that is influenced by persistent
organic pollutants, other environmental agents, genetic factors such
as susceptibility haplotypes, and by their interactions.3-6
The causal role of persistent organic pollutants in diabetes is more
likely to be contributory and indirect-eg, through immunosuppressant,
non-genotoxic, perhaps epigenetic mechanisms.3-7,11,12 A proper
understanding of how genes and persistent organic pollutants interact
to cause diabetes is important both for primary prevention and to
advance basic knowledge on diabetogenic mechanisms. When assessing the
mechanisms linking diet, fat intake, obesity, and diabetes, persistent
organic pollutants should also be considered. We need a better
understanding of the burden of diabetes that these pollutants might
contribute to cause.
I declare that I have no conflict of interest.
NOTES: AFFILIATION:
a Institut Municipal d'Investigació Mèdica, Universitat Autònoma de
Barcelona, E-08003 Barcelona, Spain;
b University of North Carolina, Chapel Hill, North Carolina, USA
References
1 DH Lee, IK Lee, K Song, A strong dose-response relation between
serum concentrations of persistent organic pollutants and diabetes:
results from the national health and examination survey 1999-2002,
Diabetes Care, Vol. 29, 2006, p. 1638-1644, .
2 O Vasiliu, L Cameron, J Gardiner, P DeGuire, W Karmaus,
Polybrominated biphenyls, polychlorinated biphenyls, body weight, and
incidence of adult-onset diabetes mellitus, Epidemiology, Vol. 17,
2006, p. 352-359, .
3 M Rewers, P Zimmet, The rising tide of childhood type 1 diabetes:
what is the elusive environmental trigger?, Lancet, Vol. 364, 2004, p.
1645-1647, .
4 D Daneman, Type 1 diabetes, Lancet, Vol. 367, 2006, p. 847-858, .
5 RB Remillard, NJ Bunce, Linking dioxins to diabetes: epidemiology
and biologic plausibility, Environ Health Perspect, Vol. 110, 2002, p.
853-858, .
6 MP Longnecker, JL Daniels, Environmental contaminants as etiologic
factors for diabetes, Environ Health Perspect, Vol. 109, Iss. suppl 6,
2001, p. 871-876, .
7 LG Hansen, Stepping backward to improve assessment of PCB congener
toxicities, Environ Health Perspect, Vol. 106, Iss. suppl 1, 1998, p.
171-189, .
8 Department of Health and Human Services, Centers for Disease Control
and Prevention, National Center for Environmental Health, Third
National Report on Human Exposure to Environmental Chemicals,
http://www.cdc.gov/exposurereport/3rd/, 2005, (accessed July 13, 2006), .
9 KS Schafer, SE Kegley, Persistent toxic chemicals in the food
supply, J Epidemiol Community Health, Vol. 56, 2002, p. 813-817, .
10 M Porta, E Zumeta, Implementing the Stockholm treaty on POPs,
Occupat Environ Med, Vol. 59, 2002, p. 651-652, .
11 A Luch, Nature and nurture-lessons from chemical carcinogenesis,
Nat Rev Cancer, Vol. 5, 2005, p. 113-125, .
12 P Alonso-Magdalena, S Morimoto, C Ripoll, The estrogenic effect of
bisphenol A disrupts pancreatic ?-cell function in vivo and induces
insulin resistance, Environ Health Perspect, Vol. 114, 2006, p. 106-112, .
A Strong Dose-Response Relation Between Serum Concentrations of
Persistent Organic Pollutants and Diabetes
Results from the National Health and Examination Survey 1999–2002
Duk-Hee Lee, MD, PHD1,
In-Kyu Lee, MD, PHD2,
Kyungeun Song, MD, PHD3,
Michael Steffes, MD, PHD4,
William Toscano, PHD5,
Beth A. Baker, MD, PHD56 and
David R. Jacobs, Jr, PHD78
+ Author Affiliations
1Department of Preventive Medicine and Health Promotion Research
Center, School of Medicine, Kyungpook National University, Daegu, Korea
2Department of Endocrinology, School of Medicine, Kyungpook National
University, Daegu, Korea
3Department of Clinical Pathology, School of Medicine, Kyungpook
National University, Daegu, Korea
4Department of Laboratory Medicine and Pathology, University of
Minnesota, Minneapolis, Minnesota
5Division of Environmental Health Sciences, School of Public Health,
University of Minnesota, Minneapolis, Minnesota
6Regions Hospital, Occupational and Environmental Medicine, St. Paul,
Minnesota
7Division of Epidemiology, School of Public Health, University of
Minnesota, Minneapolis, Minnesota
8Department of Nutrition, University of Oslo, Oslo, Norway
Address correspondence and reprint requests to Duk-Hee Lee, MD, PhD,
Department of Preventive Medicine, School of Medicine, Kyungpook
University, 101 Dongin-dong, Jung-gu, Daegu, Korea 700-422. E-mail:
lee_dh at knu.ac.kr
Next Section
Abstract
OBJECTIVE—Low-level exposure to some persistent organic pollutants
(POPs) has recently become a focus because of their possible link with
the risk of diabetes.
RESEARCH DESIGN AND METHODS—Cross-sectional associations of the serum
concentrations of POPs with diabetes prevalence were investigated in
2,016 adult participants in the National Health and Nutrition
Examination Survey 1999–2002. Six POPs
(2,2′,4,4′,5,5′-hexachlorobiphenyl,
1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin,
1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin, oxychlordane,
p,p′-dichlorodiphenyltrichloroethane, and trans-nonachlor) were
selected, because they were detectable in ≥80% of participants.
RESULTS—Compared with subjects with serum concentrations below the
limit of detection, after adjustment for age, sex, race and ethnicity,
poverty income ratio, BMI, and waist circumference, diabetes
prevalence was strongly positively associated with lipid-adjusted
serum concentrations of all six POPs. When the participants were
classified according to the sum of category numbers of the six POPs,
adjusted odds ratios were 1.0, 14.0, 14.7, 38.3, and 37.7 (P for trend
< 0.001). The association was consistent in stratified analyses and
stronger in younger participants, Mexican Americans, and obese
individuals.
CONCLUSIONS—There were striking dose-response relations between serum
concentrations of six selected POPs and the prevalence of diabetes.
The strong graded association could offer a compelling challenge to
future epidemiologic and toxicological research.
AhR, aryl hydrocarbon receptor
DDE, p,p′-dichlorodiphenyltrichloroethane
HCB, hexachlorobenzene
HpCDD, 1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin
LOD, limit of detection
NHANES, National Health and Nutrition Examination Survey
OCDD, 1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin
PCB, polychlorinated biphenyl
PCB153, 2,2′,4,4′,5,5′-hexachlorobiphenyl
PCDD, polychlorinated dibenzo-p-dioxin
PCDF, polychlorinated dibenzofuran
POP, persistent organic pollutant
SUMPOP, sum of POP levels
TCDD, 2,3,7,8-tetrachlorodibenzo-p-dioxin
TEF, toxic equivalency factor
Persistent organic pollutants (POPs) have become widespread
environmental contaminants and now represent a global problem (1). The
toxicity of these pollutants in humans and wildlife is enhanced by
their persistence in the environment and their bioaccumulation
potential in the tissues of animals and humans through the food chain
(1). POPs include a variety of man-made chemicals. Some POPs,
including polychlorinated dibenzo-p-dioxins (PCDDs), polychlorinated
dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs),
hexachlorobenzene (HCB), and several organochlorines used as
pesticides have been highlighted by international organizations as
being chemicals of concern (2).
Low-level exposure to some POPs has recently been associated with an
increased risk of diabetes (3). Prospective cohort studies of subjects
exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), the most potent
dioxin congener of POPs, or other POPs in occupational or accidental
settings have reported increased risk of diabetes, modified glucose
metabolism, or insulin resistance (4,5,6,7,8,9,10). The U.S.
Department of Veterans Affairs added type 2 diabetes to the list of
presumptive diseases associated with the exposure to dioxin-containing
Agent Orange in Vietnam (11).
However, whether similar associations exist in the general population
with lifetime exposure to very low doses of a mixture of various POPs
is not known. Given that almost everyone has measurable amounts of
POPs, the public health significance of a relation of mixed dioxins
with diabetes may be substantial despite a relatively modest
association with any individual dioxin.
TCDD-mediated diabetes might reflect decreased expression of the
insulin-responsive glucose transporter GLUT4. Several animal studies
have demonstrated a TCDD-mediated decrease in glucose transport in
vitro and in vivo (12,13,14,15,16). The stimulation of tumor necrosis
factor-α expression by TCDD in adipose tissue and other cell types
(17,18) is relevant to insulin resistance and diabetes (19–21).
Recently, a genome-wide gene expression study reported that aryl
hydrocarbon nuclear receptor translocator was most substantially
reduced in type 2 diabetic islets; dioxin is a ligand of the aryl
hydrocarbon receptor (AhR), which is a partner of aryl hydrocarbon
nuclear receptor translocator (22).
In this study, we investigated associations of prevalent diabetes with
the serum concentrations of POPs. We could not study all 49 POPs
measured in the National Health and Examination Survey (NHANES)
1999–2000 and 2001–2002 (23) because a majority of participants had
serum concentrations under the limit of detection (LOD) of many kinds
of POPs. We therefore selected six POPs
(2,2′,4,4′,5,5′-hexachlorobiphenyl [PCB153],
1,2,3,4,6,7,8-heptachlorodibenzo-p-dioxin [HpCDD],
1,2,3,4,6,7,8,9-octachlorodibenzo-p-dioxin [OCDD], oxychlordane,
p,p′-dichlorodiphenyltrichloroethane [DDE], and trans-nonachlor) for
which at least 80% of study subjects had concentrations more than the
LOD.
Previous SectionNext Section
RESEARCH DESIGN AND METHODS
The 1999–2000 and 2001–2002 NHANES (public use dataset,
http://www.cdc.gov/nchs/about/major/nhanes/datalink.htm) conducted by
the Centers for Disease Control and Prevention were designed to be
nationally representative of the noninstitutionalized U.S. civilian
population on the basis of a complex multistage probability sample.
Details of the NHANES protocol and procedures are available elsewhere
(24,25).
PCDDs, PCDFs, PCBs, and organochlorine pesticides were measured in
serum from a random one-third subsample of subjects aged ≥12 years in
1999 and 2000. In 2001 and 2002, dioxins, furans, and coplanar PCBs
were measured in a random one-third subsample of people aged ≥20
years, and organochlorine pesticides and other PCBs were measured in a
random one-third subsample of people aged ≥12 years. For this
analysis, data from the two surveys were aggregated. A total of 2,016
study participants aged ≥20 years with information on serum
concentrations of six POPs were analyzed.
The NHANES standardized home interview was followed by a detailed
physical examination in a mobile evaluation clinic or the
participant’s home. Information on demographic characteristics,
ethnicity, and medical history of diabetes was obtained in a household
interview. Information on history of diabetes included questions about
prior diagnoses of diabetes by a physician and current use of insulin
and oral hypoglycemic agents. We substituted median values of
nonsubjects for missing BMI (measured as kilograms divided by the
square of height in meters), waist circumference, or poverty income
ratio in 291 subjects; exclusion of these 291 individuals did not
change any conclusions.
Venous blood and urine samples were collected and shipped weekly at
−20°C. PCDDs, PCDFs, PCBs, and organochlorine pesticides were all
measured as individual chemicals by high-resolution gas
chromatography/high-resolution mass spectrometry using isotope
dilution for quantification. All analytes were measured in ∼5 ml of
serum using a modification of the method of Turner et al. (26). The
POPs were provided by NHANES and adjusted for serum total cholesterol
and triglycerides. Plasma fasting glucose was measured using a
modified hexokinase enzymatic method.
For each POP, the reference group was subjects with serum
concentrations under the LOD, and subjects with detectable values were
further categorized using the 25th, 50th, 75th, and 90th percentiles.
It should be noted that these analyses have an individual LOD that
varied with the extractable sample volume. Only the maximum observed
LOD was provided by NHANES. A higher sample volume results in a lower
LOD and a better ability to detect low levels of a substance. To
evaluate the summary effect of six POPs, the category number of each
POP (0 assigned to the nondetectable category, and 1 through 5
assigned to successively increasing categories) was added to make the
sum of POP levels (SUMPOPs), producing a value of 0–30, which was
itself categorized at its 25th, 50th, 75th, and 90th percentiles,
making five groups.
Participants were considered to have diabetes if 1) their fasting
plasma glucose was ≥126 mg/dl or their nonfasting plasma glucose was
≥200 mg/dl or 2) they reported a history of physician-diagnosed
diabetes. Exclusion of nonfasting subjects did not greatly change the
estimates. However, 34.5% of the 2,016 study subjects did not fast for
at least 8 h, and their exclusion substantially limited stratified
analysis. Thus, we present results based on 2,016 study subjects.
Logistic regression models were used to calculate
multivariate-adjusted odd ratios (ORs). Adjusting variables were sex,
race/ethnicity, age (years), poverty income ratio (continuous), BMI
(continuous), and waist circumference (continuous). Subgroup analyses
stratified by age, sex, race/ethnicity, poverty income ratio, or BMI
were performed. All statistical analyses were performed with SAS 9.1
and SUDAAN 9.0. Estimates of the main results were calculated to
account for stratification and clustering (27), adjusting for age,
race and ethnicity, and poverty income ratio instead of using sample
weights; this adjustment is regarded as a good compromise between
efficiency and bias (27,28). The rarity of diabetes in the least
exposed category of SUMPOPs and in the stratified analyses presented a
statistical challenge because of possible unreliability of the
absolute risk estimate at very low risk, resulting in very wide
confidence limits for ORs relative to this natural reference category.
To address this statistical problem, we present ORs for prevalent
diabetes according to SUMPOPs in two alternative formats, one using
the lowest category and one the second-lowest category as the
referent. We did not do this in the stratified analyses because the
number at risk in the different POP categories varied considerably
across strata, making the strategy of shifting referent category
confusing. There were zero cases in the least-exposed categories in
some strata, yielding an infinite OR; we conservatively estimated ORs
by artificially adding one case in those lowest exposure categories.
Previous SectionNext Section
RESULTS
Age was the closest correlate of serum concentrations of all POPs with
correlation coefficients ranging from 0.44 (HpCDD) to 0.74
(oxychlordane) (Table 1). For example, the mean age of subjects with
PCB153 nondetectable or <25th percentile was 35 years compared with a
mean age of 68 years for subjects with concentrations >90th percentile
among those with detectable concentrations. Men tended to have lower
concentrations of most POPs, especially OCDD. Both non-Hispanic white
race/ethnicity and poverty income ratio were inversely associated with
most POPs, especially DDE. After adjustment for age, the relations of
BMI with POPs were variable depending on POPs. There were significant
positive associations of BMI with HpCDD, OCDD, or DDE, whereas BMI was
inversely associated with PCB153 (Table 1). There were strong
correlations in serum concentrations among all POPs, e.g., r = 0.92
was seen for oxychlordane and trans-nonachlor, and correlation of each
of these with PCB153 was about 0.7. HpCDD and OCDD had a correlation
of 0.78. All other pairwise correlations of POPs were in the range of
0.37 to 0.53.
Prevalence of diabetes (n = 217) was unrelated to TCDD, which was
detectable in only 7% of the sample. However, diabetes was strongly
positively associated with all six POPs detectable in at least 80% of
the sample, especially PCB153, oxychlordane, and trans-nonachlor
(Table 2), after adjustment for age, sex, race/ethnicity, poverty
income ratio, BMI, and waist circumference. Additional adjustment for
triglyceride, cholesterol, saturated fat intake, and cigarette smoking
did not materially change the results (data not shown). When the study
subjects were classified according to SUMPOPs, adjusted ORs for
diabetes were 1.0, 14.0, 14.7, 38.3, and 37.3 (P for trend < 0.001)
(Table 2). After exclusion of nonfasting subjects, adjusted ORs were
1.0, 16.9, 15.8, 36.7, and 38.0 (P for trend < 0.001). Examination of
the alternate analysis using the second-lowest exposure category as
referent highlights the large increase in risk between the lowest and
second-lowest exposure categories, with a further significant 2.5-fold
increase in ORs at >75th percentile of SUMPOPs. The association
between SUMPOPs and fasting glucose levels among nondiabetic subjects
showed a weak positive trend (adjusted means 88.3, 89.5, 89.9, 89.5,
and 90.7 mg/dl, P for trend = 0.08).
After stratification by age, sex, race/ethnicity, poverty income
ratio, or BMI, the prevalence of diabetes increased with increasing
concentration category of the six POPs in most subgroups (Table 3).
Although most P values for interaction were nonsignificant, the
associations tended to be stronger among younger subjects, Mexican
Americans, and obese subjects. It was interesting that there was no
association between obesity and diabetes among subjects with
nondetectable levels of POPs, despite the substantial numbers at risk
in each BMI category.
Previous SectionNext Section
CONCLUSIONS
An inference that observed associations are causal should be made
carefully in a cross-sectional study such as this one. It may be that
metabolic changes caused by diabetes slow metabolism and/or excretion
of POPs, leading to a greater accumulation. The fact that diabetes was
associated with all six POPs investigated, despite different
toxicological profiles, could lend credence to such an alternative
possibility. However, we think that the relation between POPs and
diabetes observed in this study may be causal for several reasons.
First, our finding is basically consistent with prospective cohort
studies whose study subjects were exposed to high doses of POPs in
occupational or accidental settings, despite a difference in strength
of association (4–10). As we discuss later, the strength of
association in the current study subjects with large chronic lifetime
exposure to low doses of POPs could be stronger than in those with
short-term exposure to high doses of POPs. Second, the idea that
dioxin exposure may cause diabetes is in line with the known biology
of these pollutants. Third, reverse causality is unlikely because the
metabolism of POPs in mammalian systems is intractable; the half-life
of the compounds ranges from 7 to 10 years in humans (29,30).
Supporting our assertion, one human study reported that the rate of
elimination of POPs from blood was not associated with the duration of
diabetes (31). Fourth, the associations of diabetes with all the POPs
investigated may be reasonably explained by the high correlations
among serum concentrations of various POPs in the human body. Yet it
is entirely possible that the six POPs studied here are not themselves
causally related to diabetes. Rather, they could be surrogates of
exposure to a mixture of POPs. Finally, >90% of POPs comes from animal
foods in the general population without occupational or accidental
exposures (1), but diabetic patients tend to alter their diet toward
consuming more plant foods than animal foods. Thus, dietary changes
after diagnosis of diabetes would seem to be a negative confounder,
not a positive one. Another scientifically interesting finding was
that obesity did not increase the prevalence of diabetes among
subjects with nondetectable levels of POPs even though there were
sufficient numbers of study subjects at risk in each BMI category.
In the U.S., the serum concentrations of POPs in the general
population have been decreasing over several decades (32). Thus, the
current dramatic increase in type 2 diabetes incidence may be puzzling
if the striking association between serum concentration of POPs and
diabetes shown in this study is causal. This puzzle may be explained
by the epidemic of obesity in the U.S.; our study showed that the
association between POPs and diabetes was much stronger among obese
subjects compared with that of lean subjects. As people get fatter,
the retention and toxicity of POPs related to the risk of diabetes may
increase.
The concept of toxic equivalency factors (TEFs), a measure of ability
to bind to the AhR, has been developed to facilitate risk assessment
and regulatory control of exposure to complex PCDD, PCDF, and PCB
mixtures (33,34). However, we did not use TEFs to calculate the
cumulative effect of POPs because the strength of association of each
POP observed in this study did not appear to be correlated with the
TEF of each POP, leading us to hypothesize that binding to the AhR may
not be the critical pathway. In fact, the AhR hypothesis does not
explain all aspects of toxicity, notably the extreme variation of
toxicity between different animal species (35).
In most previous epidemiological studies (4–10), only TCDD was
evaluated as a risk factor for diabetes because TCDD is the most
potent congener of these POPs. We did not examine TCDD here because so
few individuals had detectable levels. In women and non-Hispanic
blacks in the NHANES 1999–2002, only the 95th TCDD percentiles could
be characterized, which were 6.4 and 7.4 pg/g lipid, respectively
(23). The remainder of the U.S. population is likely to have even
lower levels of this hallmark dioxin.
Dose-response relations shown in this study were surprisingly strong
compared with the weak to modest associations shown in the previous
epidemiological studies (4,5,6,7,8,9,10). Our study had two important
design features lacking in other studies: first, we selected those
POPs for which we were sure those with nondetectable levels would have
very low levels and could serve as the reference group; and second, we
evaluated a composite of POP levels. In our study, the risk of
prevalent diabetes increased consistently across the range of SUMPOPs.
In this situation, the selection of the reference group is
statistically critical to the estimated strength of ORs. For example,
if we pooled the lower four categories of POPs as the referent group
and compared it with the highest category, the OR would be
substantially underestimated. In fact, most previous epidemiological
studies on POPs were performed with subjects who had exposure to
higher concentrations of POPs in occupational or accidental settings,
taking the general population as the reference group. However, our
current result suggests that this kind of approach may not be valid
because there may be a much clearer dose-response relation in the
lower concentrations of background concentrations of POPs in the
general population. Interestingly, this observation appeared to be in
good agreement with the dose-response relation of TCDD observed in
experimental studies. According to experimental studies, the
administered dose of TCDD linearly increased the hepatic TCDD
concentrations; however, the induction of cytochrome P-450 enzymes
(CYP1A1 and CYP1A2), one of the most sensitive responses to TCDD and
its structural analogs, increased nonlinearly as a function of the
hepatic concentration of TCDD, reaching the maximum effect (36).
Similar findings were observed with some PCBs (37). Humans are
currently regarded as a less-susceptible species with respect to TCDD
or other congeners based on findings of previous epidemiological
studies with subjects having high exposure to POPs (38). However, the
chronic exposure to low concentrations of POPs in the general
population may be more detrimental in developing adverse health
effects than previously thought. Along these lines, it is worthwhile
to note that the most consistent dose-response associations between
POPs and diabetes appeared to occur in epidemiological studies with
subjects having lower serum concentrations of TCDD than in
occupational settings (4,8), conceivably because of the statistical
artifact of not identifying a true low-risk subgroup. Unlike prior
studies, in this study, we analyzed several POPs simultaneously so
that we could estimate the cumulative effect of exposure mixtures. In
most previous studies, only serum concentrations of TCDD were
measured. Although TCDD is well known to be the most potent POP
because of a strong affinity to AhR, other mechanisms might also be
involved in the toxicity of POPs for diabetes (39). Thus, other POPs,
as well as TCDD, might be relevant in the pathogenesis of diabetes.
This study has several limitations. The current findings should be
interpreted with caution because of the cross-sectional nature of this
study, despite both strength and consistency of associations. The
NHANES dataset did not allow us to differentiate type 1 from type 2
diabetes, and the association of POP levels with diabetes prevalence
might differ by diabetes type. Only 11 subjects were aged <40, so most
subjects probably had type 2 diabetes. Experimental studies have shown
that TCDD could cause hypoinsulinemia through an alteration of
pancreatic membrane tyrosine phosphorylation, suggesting that POPs may
be involved in the pathogenesis of type 1 diabetes as well as type 2
diabetes (40). Also, misclassification bias is possible because some
subjects with a higher POP value but a lower sample volume could be
classified in the reference group or vice versa. Such
misclassification would be nondifferential if (as is likely) sample
volume is unrelated to prevalence of diabetes. Finally, because
diabetes was extremely rare in those with the least exposure to POPs,
the reference category may not be stable and ORs could be overestimated.
In summary, there were striking monotonic and additive dose-response
relations between serum concentrations of six selected POPs and the
prevalence of diabetes. These cross-sectional findings, although not
definitive, are sufficiently provocative that further study should be
done. A prospective study of the relation between dioxin exposure and
diabetes is needed because both the exposure and the disease have
substantial prevalence and the public health significance could be
marked.
Previous SectionNext Section
View this table:
In this window
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Table 1—
Spearman correlation coefficients* among six POPs with age, sex, race
and ethnicity, poverty income ratio, BMI, and waist circumference
View this table:
In this window
In a new window
Table 2—
Adjusted ORs and 95% CI of prevalent diabetes by category of six POPs
View this table:
In this window
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Table 3—
Adjusted ORs and 95% CIs of prevalent diabetes by category of the sum
of six POPs after stratified by age, sex, race and ethnicity, poverty
income ratio, or BMI
Previous SectionNext Section
Acknowledgments
This research was funded by the Korea Health 21 R&D Project, Ministry
of Health & Welfare, Republic of Korea (A050349), by grant RTI04-01-01
from the Regional Technology Innovation Program of the Ministry of
Commerce, Industry and Energy (MOCIE), Republic of Korea, and by grant
R01 HL 53560 from the U.S. National Institutes of Health (to M.S. and
D.R.J.).
Previous SectionNext Section
Footnotes
A table elsewhere in this issue shows conventional and Système
International (SI) units and conversion factors for many substances.
The costs of publication of this article were defrayed in part by the
payment of page charges. This article must therefore be hereby marked
“advertisement” in accordance with 18 U.S.C Section 1734 solely to
indicate this fact.
Accepted April 5, 2006.
Received March 10, 2006.
DIABETES CARE
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g/
Indigene Völker, Diabetes und die Bürde der Umweltverschmutzung
Diabetes wird heute vielerorts als die Epidemie des 21. Jahrhunderts
angesehen. Mit ungefähr 284 Millionen Menschen, bei denen diese
Krankheit gegenwärtig diagnostiziert wurde, ist dies bestimmt keine
Übertreibung, nicht zuletzt für Indigene Völker.
Nach dem “State of the World’s Indigenous Peoples Report”, dem Bericht
über die Lage der Indigenen Weltbevölkerung der Vereinten Nationen,
haben mehr als 50% der Indigenen Erwachsenen über 35 Jahre Diabetes
Typ 2, und es heißt darin, “diese Zahlen werden voraussichtlich noch
steigen”.
Diabetes wird “Lifestyle Krankheit” genannt, für deren grassierende
Ausbreitung man Fettleibigkeit verantwortlich macht, die unserem
zunehmenden Verlass auf die westliche Ernährungsweise (auch als
Fleisch-Zucker-Diät bekannt) und unserem Verzicht auf regelmäßige
körperliche Betätigung geschuldet ist.
Während dies sicher mitverursachende Faktoren sein können, gibt es
immer mehr wissenschaftliche Belege, dass zwischen Diabetes und
unserer Umwelt ein enger Zusammenhang besteht. Es wurden über ein
Dutzend Studien veröffentlicht die langlebige organische Schadstoffe,
Persistent Organic Pollutants (POPs), darunter Polychlorierte
Biphenyle (PCBs), als Dioxine bekannte krebserzeugende
Kohlenwasserstoffe und das tödlichste synthetische Pestizid DDT, in
einen Zusammenhang mit höheren Raten der Erkrankung bringen.
„Wenn es die POPs sind, wenn nicht Übergewicht Diabetes verursacht,
ist dies wirklich heftig, wenn es stimmt“, meint Dr. David O.
Carpenter, Direktor des Institutes für Gesundheit und Umwelt an der
Universität von Albany (im Bundesstaat New York).
Einer von vier Indigenen Erwachsenen, die in Kanadischen Reservaten
leben, wurde mit Diabetes vom Typ 2 diagnostiziert, der am weitesten
verbreiteten Form von Diabetes. Die Prävalenz dieser Erkrankung
scheint dermaßen stark zu sein, dass die Zahl der in Kanada neu
diagnostizierten Fälle über dem Wachstum der Indigenen Bevölkerung
liegen könnte. Es ist nicht mehr ungewöhnlich, Kinder die nicht älter
als drei Jahre sind, mit dieser Erkrankung zu finden. Nach der
Statistik der Regierung werden 27 Prozent aller Indigenen Menschen in
Kanada in den nächsten 10 Jahren an Diabetes vom Typ 2 leiden.
Die Situation der Sandy Lake First Nation in der Sioux Lookout Zone
von Nord Ontario entspricht genau diesen Daten. Eine Studie vom März
2009, die von Dr. Stewart Harris mitverfasst wurde stellte fest, dass
26 Prozent der Gemeinschaft an dieser Krankheit leiden, die höchste in
Kanada festgestellte Diabetes-Rate. Mit einer Bevölkerung von 2.500
wurde die nördliche Cree Gemeinschaft kürzlich als ein “Epizentrum”
der Epidemie beschrieben.
Es wurde wenig über die Konzentrationen langlebiger organischer
Schadstoffe in Sandy Lake geforscht, doch nach Angaben des First
Nations Environmental Health Innovation Network (FNEHIN), (Plattform
zur Vernetzung von First Nations und Umweltmedizin-Forschung) sind von
mehreren Nachbar-Gemeinschaften die ebenfalls hohe Diabetes Raten
aufweisen, wie der Kitchenuhmaykoosib Inninuwug First Nation, erhöhte
PCB-Werte ihrem Blut bekannt.
Die Mohawk Gemeinschaft von Akwesasne muss sich auf ihre Art mit
Diabetes und der Belastung durch POPs auseinandersetzen. Ihr
Lebensraum erstreckt sich über die Staatsgrenze zwischen New York und
Ontario-Quebec entlang des St. Lawrence Flusses. Über Jahrzehnte
leiteten drei Aluminium-Gießereien stromaufwärts des Reservats PCBs in
den Fluss und verseuchten Wasser, Boden und Vegetation.
Dr. Carpenter hat sich jahrelang mit erwachsenen Mohawks in Akwesasne
wissenschaftlich beschäftigt. Erst kürzlich, im Jahre 2007, war er an
einer Studie beteiligt, die den Zusammenhang zwischen Diabetes und
Umweltverschmutzung in der Gemeinschaft untersuchte. “Unsere Studie an
erwachsenen Mohawks zeigte eine auffällige Erhöhung der Diabetes-Raten
in Abhängigkeit von den Blutwerten dreier langlebiger organischer
Schadstoffe, DDE, dem Stoffwechselprodukt von DDT, Hexachlorbenzol und
PCBs”, so Dr. Carpenter. “Unsere Ergebnisse stimmen sehr gut mit denen
von Lee et al überein.”
2006 zeigten Dr. Dae-Hee Lee und ihre Kollegen, dass für Menschen mit
der höchsten Belastung durch POPs die Wahrscheinlichkeit an Diabetes
zu erkranken ungefähr 38 mal höher ist, als für solche mit der
niedrigsten Belastung. Außerdem, “zeigten sie, dass für Personen die
zwar übergewichtig waren, aber keine hohen Werte von POPs im Blut
aufwiesen, das Risiko an Diabetes zu erkranken nicht erhöht war”,
fährt Dr. Carpenter fort. “Wahrscheinlich werden die meisten Leute
übergewichtig, weil sie zu viele tierische Fette aufnehmen und genau
in denen sind die POPs enthalten.”
Die Aufnahme von POPs über die Nahrung wurde von der Amerikanischen
EPA (Environmental Protection Agency) in ihrem Entwurf von 1994 zur
Dioxin Neubewertung bestätigt, der offiziell nie veröffentlicht worden
ist. Nach diesem Entwurf zur Neubewertung stammt 93 Prozent unserer
Dioxinbelastung aus dem Verzehr von Rindfleisch, Milchprodukten,
Milch, Geflügel, Schweinefleisch, Fisch und Eiern. Mit anderen Worten,
die westliche Ernährungsweise.
Eine im Mai 2001 im Journal für Toxikologie und Umweltmedizin
veröffentlichte Studie zog ähnliche Schlüsse aus der Neubewertung der
EPA. Zusätzlich zeigte die Studie, dass “Säuglinge sehr viel mehr
Dioxine in Relation zum Körpergewicht aufnehmen, als alle älteren
Altersgruppen” und dass Muttermilch doppelt so giftig ist wie Milch
aus dem Handel. Außerdem wurde festgestellt, dass Veganer den aller
niedrigsten Anteil von POPs in ihrem Körper aufwiesen.
Nach einer Veröffentlichung vom Oktober 2009, des Forschungszentrums
für Umweltchemie und Ökotoxikologie der Masaryk University, sind die
Weltmeere eine weitere Hauptquelle von POPs, insbesondere DDT. Darüber
hinaus wurde in der Abhandlung festgestellt, dass trotz aller
Einschränkungen, die der Verwendung von DDT vor über 30 Jahren
auferlegt wurden, die Konzentrationen des Giftes weiter zunehmen.
Indigene Völker tragen einen ungleich hohen Anteil dieser globalen
Giftlast. Nach dem National Pollutant Release Inventory (NPRI), der
staatlichen Erfassung von Schadstoffemissionen von Environment Canada,
einer Einrichtung des Kanadischen Umweltministeriums, gibt es in
Kanada beispielsweise 212 Indigene Gemeinschaften, die flussabwärts
oder in der Nähe von Zellstoff-Fabriken oder anderen Anlagen leben,
die Dioxine oder Furane abgeben. Ein erschreckendes Beispiel ist die
alte Dryden Pulp Mill in der Nähe von Grassy Narrows. Nach Auskunft
des Mercury Disability Boards, dem von den betroffenen Gemeinschaften
gebildeten Rat für Quecksilber-Behinderung, der auf gesetzlicher
Grundlage über Entschädigungsrenten für Angehörige der Grassy Narrows
und Islington Bands entscheidet, leitete dieser Betrieb von 1962 bis
1970 tonnenweise Quecksilber-Abwasser, das zusätzlich Dioxin enthielt,
in den English-Wabigoon River.
Vierzig Jahre später stellt der giftige Abfall immer noch eine
“ernsthafte Gefahr” für die Grassy Narrows und die Wabaseemoong First
Nations dar, wie das Disability Board erklärt. Zur Dekontamination
wurden von der Staats- oder Landesregierung keinerlei offizielle
Schritte unternommen.
Die Lage der Tohono O’odham Nation erinnert sehr an die Grassy
Narrows: diese Nation im Südwesten Arizonas weist die welthöchste
Diabetesrate auf. Stammeseigenen Gesundheitsbeamten zufolge wurde bei
fast 70 Prozent der 28.000 Menschen zählenden Bevölkerung diese
Erkrankung diagnostiziert. Die O’odham Angehörigen sind die
zweitgrößte Indigene Nation in den Vereinigten Staaten.
Lori Riddle gehört zur Aquimel O’odham Gemeinschaft und ist Gründerin
der Gila River Alliance for a Clean Environment (GRACE), der Gila
River Allianz für eine unbelastete Umwelt.
GRACE dient dem zehnjährigen Kampf gegen eine gefährliche
Müllaufbereitungsanlage, die ohne ausreichende Genehmigung für
Jahrzehnte auf O’odham-Gebiet in Betrieb war. Die Anlage gehörte der
Romic Environmental Technologies Corporation und spuckte
ununterbrochen Abwasser in die Luft, bis sie schließlich 2007
geschlossen wurde.
Die Anlage von Romic war nicht der erste Beitrag zur toxischen
Belastung der O’odham’s, erklärt Riddle. Sich an ihre Kindheit
erinnernd berichtet sie: “Fast ein Jahr lang, immer wenn ein Flugzeug
über unseren Köpfen geflogen ist, konnte man den Nebel sehen. Wir
dachten nie daran unser Wasser abzudecken. Die Chemikalien
bemächtigten sich unser und wurden ein Teil von uns.”
Von den frühen 50′er Jahren bis in die späten Sechzigern sprühten
Baumwoll-Farmer im Wassereinzugsgebiet des Gila Rivers routinemäßig
DDT auf ihre Pflanzen um sie gegen Baumwollraupen zu schützen. Nach
Angabe der Agentur für giftige Substanzen und Erfassung von
Erkrankungen, der Agency of Toxic Substances and Disease Registry
(ATSDR), versprühten die Farmer jährlich ungefähr 23 Pfund DDT pro
Acre, das sind etwa 25.7 Kilogramm pro Hektar.
1969 wurde im Staat Arizona der Einsatz von DDT verboten. Zu dem
Zeitpunkt war der Fluss hochgradig kontaminiert. Nach Auskunft der
ATSDR wechselten die Farmer danach zu Toxaphen, einem Ersatz für DDT,
bis dieses 1990 von der US-Regierung verboten wurde.
Wegen diesen Chemikalien, erklärt Riddle, waren die O’odham gezwungen,
ihre traditionelle Ernährung aufzugeben und die westliche anzunehmen.
Auch mussten Farmen aufgegeben werden und nötigten die Familien ihre
Stammesgemeinschaft zu verlassen. Gesellschaften wie Romic begannen,
sich auf ihrem Gebiet nieder zu lassen und trieben die Situation auf
die Spitze. “Das hat unserer Lebensqualität einen Tribut abverlangt”,
sagt sie. “Ich habe mich in den Schlaf geweint.”
Die O’odham schlagen sich mit dem herum, was Riddle als “Cluster
Symptome” bezeichnet. Das sind Fehlgeburten, Arthritis der
Wirbelsäule, Atemprobleme, unerklärliche Hautausschläge und Probleme
mit der Produktion roter Blutkörperchen. Dies zusätzlich zu Diabetes,
der häufig zu Nierenversagen, Erblindung, Herzerkrankungen und
Amputationen führt.
Es werden immer mehr Studien veröffentlicht, die in Nachfolge der
wegweisenden “Ranch Hand” Studie den Zusammenhang zwischen Diabetes
und langlebigen organischen Schadstoffen wie DDT belegen. 1998 stellte
diese Studie für US Air Force Personal, das während des Vietnamkrieges
mit dem Herbizid und Entlaubungsmittel Agent Orange besprüht worden
war, eine Zunahme von Diabetes (der eine Insulinkontrolle erfordert)
um 166 Prozent fest. Die Studie zeigte auch, dass sich mit höheren
Dioxinwerten die Häufigkeit und die Schwere von Typ 2 Diabetes
ebenfalls erhöht; die Zeit bis zur Erkrankung verkürzte sich einem
ähnlichen Trend folgend.
Dr. Carpenter weist jedoch darauf hin, dass wegen der überall auf
Zustimmung stoßenden Meinung, Diabetes sei eine durch die Lebensweise
verschuldete Erkrankung, die von der Ernährungsweise und dem Maß an
Bewegung abhängt, dem Zusammenhang mit POPs von Regierungen,
Nachrichtenagenturen oder irgend einer von den Hunderten an
gemeinnützigen Diabetes-Stiftungen weltweit, wenig Beachtung geschenkt
wird. “Nicht einmal bei uns, in Medizinerkreisen, ist dies
angekommen”, fügt Dr. Carpenter hinzu. “Man braucht viel Zeit um
beides zu ändern, die Ansichten der Medizin und die der Öffentlichkeit.”
“Das eine was jeder tun kann ist eindeutig, weniger tierisches Fett zu
essen”, empfiehlt Dr. Carpenter. Einige Indigene Gemeinschaften im
nördlichen Manitoba und in British Columbia haben damit begonnen dies
zu tun, indem sie ihre eigenen Gärten bepflanzen und Gewächshäuser
bauen; indem sie ganz traditionell auf ein paar Lebensmitteln
zurückgreifen, die sie seit Millenien versorgt haben. Andere wenden
sich körperlichen Aktivitäten zu, was nicht nur für die Prävention von
Diabetes, sondern für ihre gesamte Gesundheit eine wichtige Rolle spielt.
“Wir müssen also Wege finden, die POPs aus den Tieren
herauszubekommen, die wir essen. Das wird nicht einfach sein,
angesichts des Ausmaßes, wie verseucht wir die Welt gemacht haben”,
ergänzt Dr. Carpenter. Deshalb weist Lori Riddle, die selbst an
Diabetes erkrankt ist, auf den Tribal Council (Stammesrat) und auf die
US-Bundesregierung hin.
Autor und Copyright:
John “Ahniwanika” Schertow, Indigenous people, diabetes and the burden
of pollution, Winnipeg 02.02.2010
Zum Autor: Ahni ist ein Verfechter Indigener Rechte und Autor des
Blogs Intercontinental Cry
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Ontario Environmental Directory
http://www.oen.ca/dir/
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