Archive | May, 2011

Minimization of Exposure to Chemical Carcinogens: A Sound New Paradigm for Cancer Risk Reduction

18 May

Minimization of Exposure to Chemical Carcinogens:  A Sound New Paradigm for Cancer Risk Reduction

Donald L. Hassig, Director, Cancer Action NY; 315.262.2456; donaldhassig@gmail.com; https://preventcancernow.wordpress.com

In the past, government regulatory and public health agencies have addressed public concerns about the cancer risk imposed by exposure to chemical carcinogens by producing quantitative cancer risk assessments for individual substances and in a few instances groups of similar substances.  Quantitative cancer risk assessments describe the quantity of cancer risk imposed by exposure to a certain carcinogenic substance or group of similar substances.  These quantitative cancer risk assessments are made available to the public on government websites, including the website of the US Environmental Protection Agency, which includes such information organized as part of the Integrated Risk Information System (IRIS).  Availability on government websites has not translated into any significant degree of public awareness of the growing body of scientific knowledge, which supports the conclusion that chemical carcinogen exposure is a major contributor to cancer causation.  The existence of the quantitative cancer risk assessments on government websites creates the impression that government is carefully utilizing scientific knowledge for the purpose of protecting public health against exposures to chemical carcinogens that would impose more than an acceptable quantity of cancer risk.  This is a misleading impression.  Believing that government is using scientific knowledge to protect the public from exposures to chemical carcinogens that impose more than acceptable quantities of cancer risk is a mistake.  Members of the public who make this mistake fail to think carefully about minimizing their exposure to chemical carcinogens.  They believe that their own mental effort is not necessary because the government is taking care of this.

People are exposed to many chemical carcinogens on a frequent and regular basis.  Daily exposure is a reasonable way to think about this exposure.  Chemical carcinogens are present in the air, water and food supply.  The daily quantity of exposure to each different chemical carcinogen adds to a daily total of exposure for all of the chemical carcinogens, which have entered the body.  Total daily carcinogen exposure is what determines the quantity of cancer risk, which exists for the exposed individual.  The total cancer risk imposed is substantially greater than the risk imposed by exposure to any one of the chemical carcinogens to which one has been exposed.  It is highly probable that total cancer risk is greater than the sum of the cancer risks of the numerous carcinogenic substances to which a person has been exposed in a particular day.  This is because synergies exist that multiply cancer risk of multiple exposures.  For the average person, total daily cancer risk is of a magnitude that is unacceptable and leads to the high cancer incidence observed in the United States and other industrialized nations.

Existing scientific knowledge can be utilized to reduce cancer risk.  Government risk managers must take actions to minimize the release of chemical carcinogens into the environment, to motivate responsible parties to clean up contaminated sites and to protect the food supply from avoidable sources of contamination.  Government public health educators must set a considerable amount of pollutant carcinogen exposure reduction information before the public.  This information must include statements such as found below.

Exposure to chemical carcinogens is a major contributor to cancer causation.

Chemical carcinogens are present as contaminants of air, water and food.

Persistent organic pollutants (POPs), carcinogenic metals and volatile organic compounds (VOCs) constitute major groups of significant pollutant carcinogens.

POPs are contaminants of animal fat and for most POPs animal fat consumption is the major route of intake.

POPs are contaminants of the sediments of certain bodies of water and are also contaminants of certain waste sites.

Choosing not to reside in close proximity to POPs contaminated areas will minimize respiratory exposure to POPs.

Carcinogenic metals and VOCs are air pollutants.

Choosing not to reside in close proximity to industrial air pollution sources will minimize respiratory exposure to these substances.

Benzene and formaldehyde are VOCs that are present in the emission created by combustion of hydrocarbon fuels.

Avoiding breathing the concentrated emission cloud of machines that combust hydrocarbon fuels  will minimize respiratory exposure to benzene and formaldehyde.

Minimizing hydrocarbon fuel combustion will reduce the presence of pollutant carcinogens in the environment.

Minimizing combustion of wastes will reduce the presence of pollutant carcinogens in the environment.

In the production of manufactured goods, replacing carcinogens with non-carcinogenic substitutes will reduce the presence of pollutant carcinogens in the environment.

Exposure avoidance actions motivated by knowledge of what is presented above will reduce exposure, thereby reducing risk.  Government public health agencies exist to fulfill the mandate of protecting public health against the harm imposed by known health hazards.  It is the responsibility of all government public health entities to provide pollutant carcinogen exposure reduction education to the general public.

3/31/11 Program Notice: Quantitative Cancer Risk Assessment Science is Insufficient to Produce an Estimate of Cancer Risk for Total POPs Exposure Imposed by Consumption of Animal Fat

14 May

Program Notice

3/31/11

Cancer Action NY’s

Cancer Action News Network

Donald L. Hassig, Producer

315.262.2456

_________________________________________________________________________________________

Loving the Earth Environmental Revolution

Quantitative Cancer Risk Assessment Science is Insufficient to Produce an Estimate of Cancer Risk for Total POPs Exposure Imposed by Consumption of Animal Fat

The unedited interview is available here.

http://www.radio4all.net/index.php/program/50638

Dr. Vincent Cogliano is the scientist responsible for running the US Environmental Protection Agency’s Integrated Risk Information System (IRIS).  Dr. Cogliano describes the current state of scientific knowledge on the subject of quantitative cancer risk assessment for persistent organic pollutants (POPs). Few quantitative cancer risk assessments have been produced for POPs. At this time it is not possible to calculate an estimate of the quantity of cancer risk imposed by the total POPs exposure that results from consumption of animal fat.

The only reasonable action government public health agencies have open to them is educating the general public about POPs exposure cancer risk and exposure reduction strategies. This action has not been taken despite the fact that the federal government has been aware of POPs contamination of the food supply since the 1970s. The US government has allowed corporations to dictate silence on the subject of POPs exposure cancer risk. The government health entities must throw off all corporate control and begin immediately to educate the general public on the subject of POPs exposure avoidance via restricting consumption of animal fat.


Program Notice: Recording of 4/26/11 Cancer Action NY Public Forum on POPs Exposure Reduction

14 May

Program Notice
5/11/11

Cancer Action NY’s
Cancer Action News Network
Donald L. Hassig, Producer
315.262.2456
_______________________________________________________________________

Loving the Earth Environmental Revolution

4/26/11 Cancer Action NY Public Forum on POPs Exposure Reduction

The unedited recording of the public forum is available at the URL found
below.

http://www.radio4all.net/index.php/program/51652

A Public Forum on Persistent Organic Pollutants (POPs) Exposure Cancer

Risk and Exposure Reduction Education

Tuesday, April 26th, 2011, 7:00 PM

St. Lawrence County Human Services Building

Second Floor Conference Room

State Highway Route 310

Canton, NY

Persistent organic pollutants (POPs) are fat soluble environmental
contaminants, many of which have been classified as known or suspected human
carcinogens by government agencies, including:  the International Agency for
Research on Cancer of the World Health Organization, the US Environmental
Protection Agency and the National Toxicology Program of the National
Institute of Environmental Health Sciences of the National Institutes of
Health.  Dioxins and dioxin-like compounds, including furans and certain
PCBs are the most extensively studied POPs.  Brominated flame retardants are
an emerging group of chemicals within the POPs category.  Population wide
exposure to POPs during the course of the past seventy years appears to be a
major contributor to currently existing cancers in the industrialized world.
POPs exposure of several consecutive generations is a plausible explanation
of the occurrence of breast cancer in the 14 to 19 year old age group living
at this time.

POPs exposure reduction involves several areas of governmental activity.
Food supply monitoring can detect accidental contamination incidents such
as have recently taken place in Europe.  The removal of excessively
contaminated food from commerce is a highly important element of POPs
exposure reduction.  Increased monitoring of dioxin emission sources,
including municipal and hazardous waste incinerators will provide data that
is useful in reducing releases from these sources.  Reducing open waste
burning activity reduces POPs creation and thereby reduces POPs levels in
food.  Stopping the feeding of waste animal fat to food animals will lead to
reduced levels of POPs in meats, eggs, fish and dairy products.  Public
education on the subject of POPs exposure cancer risk and exposure avoidance
empowers individuals to make the decision to limit consumption of animal fat
foods thereby reducing their POPs exposure.

In 2010, the United Nations (UN) Environment Program (UNEP) in conjunction
with the Food and Agriculture Organization of the UN commenced a campaign to
educate the world’s citizens upon the subject of toxic and hazardous
chemical exposure disease outcome for the purpose of creating progress on
the path of transition from careless and harmful activities involving use
and disposal of toxic and hazardous chemicals to acting with responsibility.
Several categories of toxic and hazardous chemicals are addressed:  (1)
hazardous chemicals that are purposefully used in economic activity, (2)
hazardous chemicals that are by products of chemical reactions or are
created by industrial processes including, primary metals production, paper
manufacturing and combustion of mixed solid wastes of which plastics are a
component and (3) the chemicals listed in the Rotterdam, Basel and Stockholm
Conventions.  This campaign is aptly called Safe Planet.  The campaign
currently consists of an outreach on POPs body burden.  Safe Planet
additionally addresses right to know with regards to trans boundary
movements of hazardous substances.  Creating widespread awareness of the
body burden problem is a highly important step toward full utilization of
existing scientific knowledge to reduce POPs exposure disease outcome.

Safe Planet is a wonderful example of government provided public educational
outreach on POPs and metals exposure disease outcome and exposure
reduction.  In hopes of creating more such educational outreach programs
within governments at the county, state and federal level, Cancer Action NY
conducts a vigorous advocacy effort centered in the St. Lawrence River
Valley and Northern Adirondack Mountains region of New York State.  Our
public forum constitutes an important element of both our advocacy work and
our public education outreach program on POPs exposure reduction.

Ruth Lunn, PhD, Director of the Office of the Report on Carcinogens housed
in the National Toxicology Program gave a PowerPoint presentation covering
the “Report on Carcinogens” (ROC), including:  history of the ROC, process
for classifying carcinogenic chemicals and the classification of several
POPs, including, dioxin, PCBs, DDT, hexachlorobenzene,
hexachlorocyclohexane, chlordane, Mirex and Toxaphene.

Dr. Jeffrey Chiarenzelli, environmental scientist and professor at St.
Lawrence University, gave a PowerPoint presentation on the movement of PCBs
from river/lake sediments to the atmosphere.  This is an important part of
the environmental science of POPs contamination of animal fat because it
explains how PCBs, and other POPs including Mirex, which were released
largely as constituents of industrial waste water have come to exist in the
terrestrial part of the environment, contaminating forage crops and
accumulating in the bodies of herbivores.  Carnivores then consume the
herbivores, which leads to accumulation of POPs at higher levels in the
carnivores.

The Cancer Action NY Public Forum was conducted for the purpose of educating
the general public as well as policy makers on the subject of the cancer
risk reduction benefits of POPs exposure reduction.  The forum was one more
step on the path of creating educational outreach programs within federal,
state and county government health agencies that address the matter of POPs
exposure reduction for the explicit purpose of cancer prevention.

Transcript of February 24, 2011 Interview with Arnold J. Schecter, MD, U Texas at Dallas, School of Public Health: Public Health Outreach on POPs Exposure Reduction Warranted

9 May

Donald L. Hassig (DH):  Good evening, Dr. Schecter.

Arnold Schecter, MD (AS):  Good evening.

DH:  Dr. Schecter is a scientist who has devoted his career, decades,
to studying the levels of POPs, persistent organic pollutants,
chemicals like dioxins, PCBs, brominated flame retardants.  He has
dedicated much of his life to studying the levels of these chemicals
in the US food supply.  Tell us about some of your more recent
research Dr. Schecter.

AS:  What we have been looking at recently is levels of certain man
made chemicals that are toxic and in some cases persistent in humans
and in food.  For example, in the past we have looked at dioxins and
PCBs in this country in Vietnam veterans and everyone in the US we
have loooked at and others have looked at where dioxins seeem to be
contaminating all of us as do PCBs.  These are described by many as
persistent organic pollutants or POPs because they are persistent in
the environment or people.  They are toxic.  They bioaccumulate.  They
cause a number of health problems.  Lately, we have been interested in
what are now known as emerging POPs and chemicals that are similar to
the emerging POPs.  We started looking not too long ago at a certain
type of flame retardant, PBDE, polybrominated diphenyl ether.  We
looked first in nursing mothers’ breast milk, because of reports from
Sweden that the levels of these were going up.  At the same time,
dioxin levels and PCB levels were decreasing in the people they
studied.  We did a study here in Texas.  We found that every nursing
mother had milk that was contaminated with PBDE type flame retardants.
By comparing it with other countries we found that the levels were
higher than had been measured in any other country.  We had three
findings.  PBDEs are in nursing mothers’ breast milk.  The levels are
the highest in the world.  We found no one who did not have this
contamination.  We realized that this meant that babies before birth
were being contaminated as some moved through the placenta.  We
realized that if an infant was getting all of his or her food by
nursing that child was going to be getting a dose of PBDEs and flame
retardants are not what babies need in their bodies.  We later looked
at PBDEs in food and found that some foods particularly with animal
fats, whether they were animals or fish or dairy products were
contaminated with PBDEs.  These are fat soluble chemicals.  When we
looked at fish with higher fat levels like salmon or sardines we found
higher levels of PBDEs.

We also were interested in looking at another popular brominated flame
retardant.  In America we use more PBDEs than in most other countries.
Another brominated flame retardant, which is believed to be toxic,
hexabromocyclododecane, was found at the same levels in nursing
mothers‘ breast milk in the US as in Europe.  The levels are lower
than PBDEs in the US but we did find them in the milk of every woman
that we looked at.  We then looked at hexabromocyclododecane in food
purchased from American supermarkets.   We found that a number of
foods were contaminated with hexabromocyclododecane.

We also were interested in perfluorinated chemicals.  We looked in
foods.  These are chemicals found in Teflon and ScotchGuard that
resist stains or resist water.  We found that a number of foods had
some of these perfluorinated chemicals.

We looked at dust vacuumed from floors in the US and Germany.  We
found that PBDEs were at fairly high levels in dust and also that they
were much higher in the US than in Germany in a small study that we
did there.

DH:  How do the PBDEs get from where they are put when used in
manufacturing?   How do they get out of the material good into the
dust and get into the food?

AS:  Yes, a very key question, of course.  What is believed now is
that PBDEs, which are found in electronics and also in mattresses,
sofas, chairs, break off from what they are put in so that if your
were to lie down on your mattress tonight if PBDEs were used to
prevent fire, then as you lie down on the mattress this may release
dust containing PBDEs.  Food also somehow gets contaminated.  I do not
know what the route is for getting into the food.

DH:  I have been familiar with this to the extent that I understand
how dioxins get into the animal food supply.  It is my understanding
that minute particulates settle upon the vegetation or the aqueous.
In the terrestrial, when these particles settle upon vegetation cattle
consume the forage that has minute particles that contain dioxins
which then accumulate in their bodies.  I wondered about the PBDEs.
Is it possible that the PBDEs would be minute particles in the outdoor
atmosphere and that they would come down like that?

AS:  Well, the PBDEs are not chemically bound to the products that
they are in.  They are added so that they can break off.  The plastic
could break off with the PBDEs.  It is not as well worked out right
now how PBDEs are migrating through the environment, food and us as
what we seem to know about dioxins.

DH:  What is known about the health impacts?  With babies that are
during gestation being exposed to PBDEs and then after gestation they
begin their own individual life and they are nursing the mother
getting more PBDEs.  Then they are in the house  crawling around on
the floor in the dust with the PBDEs.  What is know about the health
impacts of these exposures?

AS:  This is a relatively new field where investigations have been
done on laboratory animals like rats and mice and now more recently on
people, human epidemiology studies.  It is interesting that PBDEs seem
similar in some of the health outcomes to PCBs.  For example, it is
believed that both can cause cancer, both PCBs and PBDEs.  It is
believed that both can have effects on the nervous system such as
lowering IQ if the baby has been exposed or the child has been
exposed, or emotional changes in children.  Endocrine disruption,
changes in the levels of hormones.  Problems with reproduction or
development such as less fetuses carried to normal delivery;
spontaneous abortions can happen.  As best we know now, these POPs,
the PBDEs seem somewhat similar to PCBs.  The literature now is coming
out with new papers very frequently on various POPs or chemicals that
are sort of like POPs but are not POPs.  For example, bisphenol-A,
which is not persistent, but because we get an intake into our body
every day it’s something like POPs we’ve got it in us and we are
getting it in us.  So BPA which is not persistent is sometimes called
a POPs-like chemical.

DH:  I see.  Because it is continuously present in our body.  It
doesn’t persist, but by being constantly exposed it is continuously
present in our body.

AS:  Exactly.

DH:  We have talked about the presence of these chemicals, where they
are at and that they end up being part of the human body and that
there is some scientific knowledge about the diseases that can be
associated with these exposures.  Is there sufficient scientific
knowledge and this would be your expert opinion?  Is there sufficient
scientific knowledge on the subject of POPs exposure and disease
outcome to create, to produce  public health statements on these
chemicals?

AS:  There are POPs networks that have been producing public health
statements warning about health hazards.  There is an international
POPs network and the Stockholm Convention meets periodically.  (The
Stockholm Convention) targeted first what they call the “Dirty Dozen”
and has been adding to it.  For example PBDEs went on the list
relatively recently.  I think both persistent organic pollutants and
endocrine disruptors, some of which are the same chemicals have been
described by many people and many organizations as being a public
health hazard.

DH:  What is the public health message that exists in the scientific
literature from your viewpoint?

AS:  Ok. I will give you my personal opinion as someone who works in
the field.  Different scientists will not alway agree on how toxic
something is or almost anything else in science there are areas of
disagreement.  My own personal feeling is that these are man made
chemicals and they are toxic and bioaccumulate so they present a
hazard.  If at all possible, we should be using non-hazardous
chemicals or phasing out those we know to be hazardous and trying to
replace them, if we need to replace them with less hazardous
chemicals.  It may be that we could use other materials in our
mattresses to make them soft and flame resistant where you don’t need
to add man made chemicals.

DH:  This is kind of a regulatory matter, where we’re deciding what
chemicals to use.  What about the public health matter, this matter of
what do you tell the people?  What would you tell the public about
POPs?

AS:  I think I would find myself in the group of scientists who feel
that if you have something that is toxic and persistent and man made
that you don’t necessarily have to use that we should do whatever we
can do to decrease the amount in the environment and in people, but
also be thoughtful about what we replace the dangerous chemicals with.
We don’t want to replace one dangerous chemical with another.  We
want to make sure that before a new chemical is introduced that it has
been thoroughly tested for safety.

DH:  Considering the fact that numerous POPs are contaminants of
animal fat, what is the public health message on POPs that exists in
the science?

AS:  Well I think that raises a very interesting point.  What you just
mentioned is that some of the POPs are fat soluble and they are found
in animal fats.  In public health and medicine for quite some time now
there has been a general consensus among most that the less animal
fats the better for a person’s health, whether we are talking about
colon cancer, heart attacks, or heart disease, or strokes.  Now we can
add one more reason to eat less animal fat and perhaps more vegetables
and fruits and that is to decrease the intake of toxic POPs,
persistent organic pollutants or other toxic chemicals.

DH:  What would the likely outcome be of reducing your exposure to
these chemicals?  Isn’t it the point of this being addressed by public
health that having less of these chemicals in your body, less body
burden of POPs would reduce disease risk for some of these chronic
diseases?

AS:  The way I see it as a public health physician who does research
and practice in the field, in my opinion, what is happening when we
reduce toxic chemicals whether it is lead in gasoline or cigarette
smoke or dioxin, or mercury at high levels or lead at certain levels,
is that we will be reducing in the population disease.  It does not
mean that every person who ingests a certain number of molecules of a
toxic chemical is going to get sick.  It does mean that in the general
population of the six billion people on the Earth or 360 million
living in America, whatever the figure is these days, there should be
less disease and better health.

DH:  I am very hopeful that your research and the research of others
will lead to wide spread public knowledge of these matters.  We do
this work.  Our organization makes it our practice to conduct
information tables at colleges and in high schools and educate policy
makers.  We have been educating town board members all around St.
Lawrence County where our group is located, where we started up.  We
are finding that there is an interest.  People want to reduce the
incidence of these diseases, particularly cancer.  We go to a town
board and talk to them about POPs and the cancer risk that is
associated with exposure to chemicals like dioxins and PCBs.  We have
been hesitant to say very much about the cancer risk associated with
the PBDEs, just because as you say its a newer field of research and
there is not as much known about cancer outcome.  I don’t think there
is any epidemiology on cancer outcome with PBDE exposure.  There is so
much epidemiology on cancer outcome with dioxin exposure and a little
less with PCB exposure.

We go to town boards.  They have been quick, in wanting to reduce
cancer burden in their jurisdictions, they have been quick to show
their support by passing resolutions and speaking with people at other
levels of government.  They show their support for public education on
reducing exposure to POPs by way of limiting animal fat intake.  They
want the federal government, the state government and the county
governments to provide this kind of education to the general public.
We tell them that the environmental groups can not get this job done.
We need to have good partners with government to educate the public
about the existence of POPs in the food supply.

It is so good you have this great science that you produce and the
other scientists have been producing.  Let’s just step back from this
a bit.  Tell about the book that you wrote so long ago and tell us
when it was first published and how many editions it has gone through.
This book is titled, “Dioxins and Health”.  I remember checking that
out of the library quite a long time ago so I know there is quite a
bit of history here.

AS:  What is your question?

DH:  Tell us about what motivated you to write “Dioxins and Health”,
when you first published this book.  Tell us about that book.  I see
that as the Bible of POPs. It was the starting point.  It was a very
important document in the world scientific community, human beings,
dealing with the presence of these persistent organic pollutants in
the environment, in our bodies, in food.  Tell us about your work that
went into publishing “Dioxins and Health”.

AS:  The history of that, and we are working on the third edition now,
was that I went to a number of meetings both of citizens’ groups and
scientists and I noticed a great interest in the chemicals, the
dioxins, PCBs, similar chemicals.  I noticed a couple of things.  One
was even the best scientists did not understand the science that
scientists in different fields were generating.  Chemists did not
understand epidemiologist.  Physicians spoke to other physicians, not
chemists, not toxicologists who studied animals.  I thought it would
be useful to try to edit.  I didn’t write the book, I edited it to
have a book that spoke to different people and scientists to people
who are not scientists and vice versa.  That was the origin.

DH:  Great idea.  Certainly wonderful that you conceived of that and
set about doing it.  When was the first edition published?

AS:  I don’t remember.  The second edition was published in 2003.  We
are working on the third edition right now.

DH:  When do you think it will become available?

AS:  I hope it will be out before this year is over.  If not this year.
DH:  I certainly would like to know when it comes out.

AS:  We’re trying.

DH:  What changes have you seen?  What is the difference between
edition three and edition one or edition two?  What is the trend?
What has taken place in the existing scientific knowledge with regards
to dioxins and dioxin-like compounds, including some of the PCBs?

AS:  I think, well, I know we have more science on the dioxins and
PCBs.  I think what needs to be added in addition is the emerging
persistent organic pollutants such as we have been talking about or
compounds related to them.

DH:  So, in the third edition you are going to address PBDEs and the
other brominated flame retardants?

AS:  Yes.

DH:  It has been great talking to you.  I always enjoy these
interviews with you.  There is one thing more that comes to my mind,
if you have time to discuss this.  You had looked at the levels of
POPs, specifically, dioxins in the bodies of vegans and compared this
to the levels of these chemicals in the bodies of those who consume.
I am sure that you know and that most of the people in the audience
know.  Just for the completeness of this.  The term vegan refers to
the fact that people do not consume any animal products.  So you
looked at the levels of dioxins and possibly some other POPs in the
bodies of people who do not consume animal products and then you
compare that to the body burdens of these chemicals in people who do
consume animal products.  What did you find?

AS:  What we found in two small studies, one with dioxins in vegans,
or people who have not eaten any meat or fish or dairy products for a
long time, or eggs, and then with PBDEs, was that the levels were
lower in vegans than in the US general population.  In the more recent
study with PBDEs, what we found was that the longer the time since
eating meat or, animal fat, lets put it that way, the lower the
levels.

DH:  That’s certainly interesting.  It proves out this matter of if
you recommend that people reduce their intake of animal fat that the
hope is that it would cause these levels to be lower.  Then you see
this actually existing in the case of the vegans who have not been
consuming animal fat and they have these lower levels.  They certainly
are an example of how one might go about minimizing their body burden
of chemicals like dioxins and PCBs and the brominated flame
retardants.

I think I have covered everything that I wanted to talk to you about.
I look forward to these interviews with you so much because I know you
are this great source of scientific knowledge on this subject area.

What do you intend?  You told me that you were working on a research
proposal earlier today.  What are your intentions for future research
in this area, Dr. Schecter?

AS:  I would like to continue learning what levels of toxic chemicals
are in people and in food.  How does it get into us?  And then, what
is the health consequence of these chemicals?

I’m about talked out.  My voice is about gone.

DH:  Thank you so much, Dr. Schecter.  You are a great man.  I am so
glad that you are a former New Yorker.  We’ll always be able to say
that even though it’s sunnier in Texas, this is where Arnold Schecter
started his dioxins and his PCBs and his PBDEs research.    We are
very proud of that.

AS:  Thank you for your kindness and thank you for your probing,
interesting and insightful questions.

DH:  Thanks for all the research you are doing.  The research is the
very heart of the activism and the public health.  It all comes down
to what do we know.  What do the scientists know about these chemicals
and about the health of the human beings and the animals?  Thanks a
lot.

AS:  Thank you for your interest.

DH:  Have a wonderful evening.

AS:  Thanks, same to you.

UTILIZATION OF QUANTITATIVE CANCER RISK ASSESSMENT TO ASSIST DECISION MAKING ON PUBLIC HEALTH AND POPS EXPOSURE

9 May

Introduction:

Existing scientific knowledge on the subjects of persistent organic
pollutants (POPs) exposure and quantitative cancer risk assessment is
sufficient to support the provision of public health educational
outreach on the subject of POPs exposure reduction.  Government public
health entities are currently failing to provide such educational
outreach.  Advocacy for governmental educational outreach programs on
the subject of POPs exposure reduction is warranted.

Materials and Methods:

This paper was created as a result of becoming knowledgeable on the
subjects of quantitative cancer risk assessment and persistent organic
pollutants (POPs) exposure.  The process of developing that knowledge
depended in large part upon having internet access to the scientific
research literature and governmental reports addressing these
subjects.

Results and Discussion:

Beginning in the early 1900s, the entire biosphere has gradually
become contaminated with persistent organic pollutants (POPs). POPs
are persistent, man made, toxic substances.  Many of the POPs are
classified as know to cause cancer in humans or reasonably anticipated
to cause cancer in humans.

POPs are contaminants of all animal fat.  Exposure takes place largely
through consumption of animal fat.  All humans bear a body burden of
POPs.  This has been the case for several generations. Gestational
exposure has taken place repeatedly, creating a current generation
that has been shaped to a considerable extent by whatever genetic and
morphological changes are imposed by gestational POPs exposure.  In
animal studies gestational POPs exposure predisposes offspring to
increased cancer susceptibility.  It is reasonable to suspect that
gestational POPs exposure contributes to the breast cancer cases that
are now being diagnosed in girls throughout the United States.  Breast
cancer in the 14 to 19 year old age group is a new phenomenon.
Consecutive generations of gestational POPs exposure is also a new
phenomenon.

Governments around the world have failed to warn their citizens of the
POPs contamination problem.  This has happened because of the
tremendous amount of influence that corporations exert over
government.  The corporate polluters will not allow government public
health agencies to inform the public about POPs contamination of the
food supply and the damages to heath that are associated with POPs
exposure.

Government environmental health agencies have produced quantitative
cancer risk assessments for a few of the POPs.  A quantitative cancer
risk assessment is a document that describes the use of
epidemiological research findings to develop estimates of how much
cancer is caused by exposure to various quantities of a carcinogen.
Cancer incidence in low, medium and high exposure groups is plotted
against the quantities of exposure.  The slope of the line that best
approximates this data is called the cancer slope factor.  The cancer
slope factor is a number that describes the amount of cancer caused by
a unitary quantity of exposure to the carcinogen.  Multiplying the
quantity of exposure by the cancer slope factor yields an estimate of
the amount of cancer risk imposed by that particular quantity of
exposure.

The US EPA has developed a process for making available to the public
the limited risk information.  EPA’s Integrated Risk Information
System (IRIS) is accessible on the agency’s web site.

Very little scientific knowledge exists upon which to base
quantitative cancer risk assessments for the vast majority of POPs.
It is not possible at the current state of scientific knowledge to
produce quantitative cancer risk assessments for all of the POPs that
one is exposed to as a result of animal fat consumption. Thus, POPs
exposure imposes an unknown quantity of cancer risk.  However, by
simply taking into account the quantity of cancer risk that is imposed
by exposure to those POPs for which quantitative risk assessments
exist it is clear that more than an acceptable amount of cancer risk
is imposed by total POPs exposure.

Dioxin exposure cancer risk has been quantified by US EPA in Part III
of the Agency’s 2003 draft dioxin reassessment. 1 This risk is greater
than 1 in 1000 for current background levels of exposure.  However,
due to the EPA’s failure to finalize the draft dioxin reassessment, no
quantitative cancer risk assessment information for dioxin is
available through the IRIS program.  Greater than 1 in 1000 is an
unacceptable quantity of cancer risk.  Quantitative cancer risk
assessments have been produced by IRIS for several of the POPs,
including:  Chlordane, DDE, DDT, Dieldrin, Hexachlorobenzene,
alpha-Hexachlorocyclohexane and Toxaphene.  The oral exposure cancer
slope factors for these substances are provided below.  Multiplying
the quantity of exposure by the cancer slope factor produces an
estimate of cancer risk.

Chlordane 3.5 x10-1 per mg/kg-day
DDE 3.4 x10-1 per mg/kg-day
DDT 3.4 x10-1 per mg/kg-day
Dieldrin 1.6 x10-1 per mg/kg-day
Hexachlorobenzene 1.6 per mg/kg-day
alpha-Hexachlorocyclohexane 6.3 per mg/kg-day
Toxaphene 1.1 per mg/kg-day

In order to calculate the cancer risk imposed by exposure to each of
the substances listed above it is necessary to determine how much
exposure is taking place on a daily basis.  Analysis of animal fat
foods for POPs contaminants is the process that generates the basic
exposure data needed.  However, such testing is not being conducted to
the extent that reliable data is available.

No scientific knowledge exists on the subject of synergies that cause
multiple POPs exposure to impose more than an additive quantity of
cancer risk.  Simply adding the cancer risk for those POPs that have
been assessed is likely to produce an underestimate of actual cancer
risk.

The only reasonable course of action open to public health departments
is warning the public of the significant and unquantified cancer risk
imposed by the POPs exposure resultant from animal fat consumption.
The United Nations’ Safe Planet Campaign has begun to educate citizens
of the world on the subject of POPs body burden.  Hopefully, Safe
Planet will soon begin to set before the public the facts of POPs in
the food supply and the unacceptable quantity of cancer risk that this
contamination imposes.

Advocacy for provision of POPs exposure reduction educational outreach
programs by national and regional government health entities is very
much needed at this time.  Without such advocacy, government health
entities will continue to avoid the POPs exposure issue and the public
will continue to consume animal fat at unsafe levels due to lack of
knowledge concerning POPs exposure cancer risk.

Acknowledgements:

Cancer Action NY is a grassroots environmental protection/cancer risk
reduction organization.  I serve as director of this small group of
dedicated individuals because I believe in doing this work.  I am able
to do this work because of the frugality and generosity of my father,
William John Hassig, DVM.

References:

1. U S Environmental Protection Agency. (2003 Draft) “Exposure and
Human Health Reassessment for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin and
Related Compounds”. www.epa.gov

SCIENTIFIC KNOWLEDGE SUPPORTS THE CONCLUSIONS THAT PERSISTENT ORGANIC POLLUTANTS (POPs) EXPOSURE IS A MAJOR CONTRIBUTOR TO CANCER CAUSATION AND THAT POPs EXPOSURE REDUCTION EDUCATION WOULD EMPOWER BEHAVIOR CHANGES LEADING TO SIGNIFICANT REDUCTIONS IN CANCER INCIDENCE

9 May

Introduction:

Scientific knowledge has accumulated during the course of the past
several decades so as to provide a basis for concluding that exposure
to persistent organic (hydrocarbon) pollutants (POPs) is a major
contributor to cancer causation.  Now is the time for making use of
this knowledge by way of public educational outreach on POPs exposure
reduction.

Materials and Methods:

The work of creating this paper was conducted via reading and
understanding scientific research articles and government
publications.  The availability of these documents on the internet has
greatly facilitated this work.

Results and Discussion:

In the industrialized world, cancer incidence is relatively high.
Cancer is the number one cause of death worldwide.  The American
Cancer Society has reported that one in two men and one in three women
will develop cancer during their lifetime.  When one observes the
relative uniformity of the existence of high cancer incidence
throughout the industrialized world, it is reasonable to conclude that
the major sources of causation are similar for the global population.
Even in a “hot spot”, the majority of cancers are very likely to be
caused by the same exposures that are causing the majority of cancers
in the rest of the industrialized world.  Exposure to POPs, which
takes place as a result of consumption of animal fat is widespread and
involves a relatively large quantity of pollutant carcinogen intake.
It is reasonable to conclude that POPs exposure is a major contributor
to cancer causation in the industrialized world.

The excess amount of cancer that exists in a “hot spot” can be
attributed to unique exposures occurring in the “hot spot”.  The
excess cancer incidence that exists in a particular “hot spot” is
likely to result from the unique exposures that occur there:  living
downwind from large facilities that emit pollutant carcinogens into
the atmosphere, living downstream from large facilities that discharge
pollutant carcinogens into surface waters, living in the vicinity of
hazardous waste disposal sites, etc.

POPs are contaminants of all animal fat due to the lipophilic
character of these substances. Chlorinated dioxins, furans and
dioxin-like PCBs are the most studied of POPs.  Much of the scientific
research literature describes findings involving these substances.
Polybrominated diphenyl ethers (PBDEs), other brominated flame
retardants, hexachlorobenzene, hexachlorocyclohexane, Mirex,
Toxaphene, chlordane, DDT, and numerous other pesticides are also
POPs.  The limited research that exists for these substances indicates
that they are carcinogenic and that they are endocrine disruptors.
Adverse health effects including cancer are imposed via gestational
exposure and the exposures that take place during the lifetime of the
independent organism.

Several epidemiological studies have been conducted for populations
with excess dioxin exposure.  The 1976 chemical production facility
explosion that occurred in Seveso, Italy released a large quantity of
dioxins, resulting in widespread exposure of the regional population.
Occupational exposures have taken place among workers engaged in the
production of phenoxy acid herbicides, particularly in the case of
manufacture of 2,4,5-T.  Additionally, United States military forces
received excess exposure resultant from the aerial spraying of
defoliants containing dioxin contaminants during the Vietnam War.

In the 2002 paper titled, “Serum Dioxin Concentrations and Breast
Cancer Risk in the Seveso Women’s Health Study”, researchers Marcella
Warner et al reported a statistically significant positive association
between serum dioxin levels and breast cancer risk.1  The group of
women with highest blood serum dioxin concentrations exhibited a
higher rate of breast cancer incidence than groups with lower serum
dioxin levels.

Several cohorts of factory workers employed in  the manufacture of the
penoxy acid herbicide, 2,4,5-T, have been assessed for dioxin exposure
cancer outcome.  Becher, et al published the paper, “Quantitative
Cancer Risk Assessment for Dioxins Using an Occupational Cohort” in
1998.2  The authors reported a statistically significant link between
dioxin exposure and cancer mortality.  Mathematical modeling of the
data led this team to conclude that dioxin exposure cancer risk was of
a magnitude existing in the range 1 x 10 E-3 to 1 x 10 E-2 for
exposure in the amount of 1 pg TCDD/kg body weight/day.  Other
research groups have investigated cancer mortality among herbicide
production and application workers.  The results of these studies
serve to create consensus on the connection between dioxin exposure
and elevated cancer risk.

Operation Ranch Hand was the code name for US military activities
involving aerial spraying of defoliants during the Vietnam conflict.
Agent Orange, a defoliant containing relatively high concentrations of
dioxins, was utilized extensively.  In 2004, Akhtar et al published
the study titled, “Cancer in US Air Force Veterans of the Vietnam
War”.3  Increased incidence of melanoma and prostate cancer were
positively associated with dioxin exposure.

Animal studies have demonstrated that a relation exists between
gestational dioxin exposure and increased breast cancer susceptibility
in female offspring.4,5  A study published in 2008 reported delayed
initiation of breast development in girls with higher prenatal dioxin
exposure.6  These research results provide a plausible explanation of
the breast cancer cases, which have been diagnosed among American
girls as young as ten years of age during the 2000s.

Certain reports produced by United States federal government agencies
contain scientific information supporting the conclusion that POPs
exposure is a major contributor to cancer causation.  However, no US
government report provides a comprehensive analysis of the cancer risk
imposed by the POPs exposure resultant from consumption of animal fats
contaminated at current background levels.

The Agency for Toxic Substances and Disease Registry (ATSDR) published
a Toxicological Profile for Dioxins in 1998.7  At the same time, ATSDR
also published a companion document, titled “Public Health Statement
on Dioxins”.  These documents recommend reduced animal fat consumption
due to the existence of scientific knowledge describing associations
between dioxin exposure and increased cancer risk.

The United States Environmental Protection Agency (EPA) has been
endeavoring to produce a reassessment of dioxins since April 1991.
The most recent draft of the reassessment, titled, “Exposure and Human
Health Reassessment for 2,3,7,8-Tetrachlorodibenzo-p-dioxin and
Related Compounds” is dated 2003.8  The EPA draft dioxin reassessment
is a highly detailed compilation of dioxin exposure and adverse health
effects science.  According to the EPA, over 95 percent of dioxin
exposure takes place as a result of animal fat consumption.

Part III of the dioxin reassessment provides a mathematical
determination of dioxin exposure cancer risk.  EPA’s choice of a
linear model for dioxin exposure cancer risk is supported by research
findings reported in 2003 by Mackie, et al.9  The Mackie study found
no evidence of a threshold for dioxin exposure cancer risk.  Utilizing
the US EPA’s cancer slope factor it is possible to calculate
approximate population level cancer risk for dioxin exposure.  For the
US population of 308 million, dioxin exposure will cause approximately
308,000 cancer deaths in 70 years. The quantity of exposure used in
the calculation of this quantity of cancer mortality is 1 pg dioxin
TEQ/kg bw/day.

The Institute of Medicine (IoM) of the National Academies published
the report titled, “Dioxins and Dioxin-Like Compounds in the Food
Supply:  Strategies to Decrease Exposure” in 2003.10  This report
presents several strategies for reducing dioxin exposure.  A key
recommendation is that girls and women of child-bearing age reduce
consumption of animal fat containing foods so as to reduce their
dioxin exposure.  This group was given particular attention due to the
health damaging effects imposed by gestational exposure.  The IoM
report did not address dioxin exposure cancer outcome.  Its
recommendations were based upon findings of other diseases endpoints.

To make use of existing scientific knowledge for the purpose of
reducing cancer incidence to a minimum, it is essential that the
general public be provided with the following information:  the names
of the carcinogenic POPs and exhaust constituents, the places where
these pollutants exist in the environment, and strategies to avoid
exposure to these carcinogens.  It is the responsibility of government
public health agencies to provide this information to the public in an
effective and timely manner.  Posting health hazard advisories in the
market places, in supermarkets and at gas stations, would be highly
effective in building this cancer prevention public knowledge.

A simple public health message is evident in the existing scientific
knowledge.  POPs are toxic.  POPs exposure causes cancer.  Nearly
everyone bears a body burden of POPs.  POPs are contaminants of animal
fat.  Reducing animal fat consumption reduces POPs exposure thereby
lowering cancer risk.

Acknowledgements:

Cancer Action NY is a grassroots environmental protection/cancer risk
reduction organization.  I serve as director of this small group of
dedicated individuals because I believe in doing this work.  I am able
to do this work because of the frugality and generosity of my father,
William John Hassig, DVM.

References:

1. Warner M, et al. Serum dioxin concentrations and breast cancer risk in
the Seveso Women’s Health Study. Environmental Health Perspectives.
(2002) July; 110(7): 625–628.

2. Becher H, et al. Quantitative cancer risk assessment for dioxins using
an occupational cohort. Environmental Health Perspectives. (1998)
April; 106(Suppl 2): 663–670.

3. Akhtar FZ, et al. Cancer in US Air Force veterans of the Vietnam War.
Journal of Occupational Environmental Medicine. 2004 Feb;46(2):123-36.

4. Fenton SE, et al. Persistent Abnormalities in the Rat Mammary Gland
following Gestational and Lactational Exposure to
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). Toxicological Sciences 67,
63-74 (2002)

5. Jenkins S, et al. Prenatal TCDD exposure predisposes for mammary
cancer in rats. Reproductive Toxicology. (2007) Apr-May;23(3):391-6

6. Leijsa MM, et al. Delayed initiation of breast development in girls
with higher prenatal dioxin exposure; a longitudinal cohort study.
Chemosphere Volume 73, Issue 6, October (2008), Pages 999-1004

7. The Agency for Toxic Substances and Disease Registry. (1998)
Toxicological Profile for Dioxins. www.atsdr.gov

8. U S Environmental Protection Agency. (2003 Draft) “Exposure and Human
Health Reassessment for 2,3,7,8-Tetrachlorodibenzo-p-Dioxin and
Related Compounds”. www.epa.gov

9. Mackie D, et al. No Evidence of Dioxin Cancer Threshold. (2003)
Environmental Health Perspectives 111:1145-114

10. The Institute of Medicine of the National Academies of Sciences.
“Dioxins and Dioxin-Like Compounds in the Food Supply:  Strategies to
Decrease Exposure”. (2003). www.nas.edu