From greenla@umich.edu Mon Nov  7 20:39:51 EST 1994
Article: 86839 of sci.med
Path: bigblue.oit.unc.edu!concert!gatech!gt-news!cc.gatech.edu!darwin.sura.net!jhunix1.hcf.jhu.edu!jobone!newsxfer.itd.umich.edu!news.itd.umich.edu!212.40.med.umich.edu!user
From: greenla@umich.edu (Lee Green MD MPH)
Newsgroups: sci.med
Subject: Re: Why is testicular cancer increasing?
Date: 30 Oct 1994 23:11:39 GMT
Organization: University of Michigan
Lines: 38
Message-ID: <greenla-3010941913080001@212.40.med.umich.edu>
References: <1994Oct28.165932.3706@emba.uvm.edu> <38s2pr$9dg@dartvax.dartmouth.edu>
NNTP-Posting-Host: 212.40.med.umich.edu

In article <38s2pr$9dg@dartvax.dartmouth.edu>,
Gregory.W.Froehlich@dartmouth.edu (Gregory W. Froehlich) wrote:

> In article <1994Oct28.165932.3706@emba.uvm.edu>
> gdavis@griffin.emba.uvm.edu (Gary Davis) writes:
> 
> > Does anyone have any further information on this potentially catastrophic
> > problem?
> > 
> 
> I'd start by asking myself if I had any reason to think that population
> statistics on prevalence of testicular cancer, etc. were collected any
> differently today than 50 years ago. (Almost certainly).
> 
> Then I'd ask whether the diagnostic methods for testicular carcinoma
> are different now than 50 years ago (They are).
> 
> Then I'd ask, how might these differences cloud my perception of what's
> going on? (And then try to take those biases into account).
> 
> ------------------
> Greg Froehlich, MD
> White River Junction, VT

I'll second those, good suggestions all.  Comparisons of disease incidence
over time are fraught with methodological peril.  That understood, the
leading hypothesis IF the effect is real is dioxins.  It turns out they
have estrogenic effects in extremely tiny concentrations, and they're
byproducts of a wide variety of manufacturing processes.  Their effect
apparently occurs during critical stages of embryological development.

-- 
Lee Green MD MPH        Disclaimer: Information for general interest
Family Practice         and discussion only.  I can't examine you via
University of Michigan  the Internet, so you should ALWAYS consult
greenla@umich.edu       your  personal physician.  These posts are my
                        personal doings, not a service of nor the
                        responsibility of the University of Michigan.


From russ@pmafire.inel.gov Mon Nov  7 20:40:53 EST 1994
Article: 87059 of sci.med
Newsgroups: sci.med
Path: bigblue.oit.unc.edu!concert!gatech!howland.reston.ans.net!EU.net!uunet!pmafire!russ
From: russ@pmafire.inel.gov (Russ Brown)
Subject: Re: Why is testicular cancer increasing?
Message-ID: <1994Nov2.175931.8708@pmafire.inel.gov>
Date: Wed, 2 Nov 94 17:59:31 GMT
References: <1994Oct28.165932.3706@emba.uvm.edu> <38s2pr$9dg@dartvax.dartmouth.edu> <greenla-3010941913080001@212.40.med.umich.edu>
Organization: WINCO
Lines: 56

In article <greenla-3010941913080001@212.40.med.umich.edu>,
Lee Green MD MPH <greenla@umich.edu> wrote:
>In article <38s2pr$9dg@dartvax.dartmouth.edu>,
>Gregory.W.Froehlich@dartmouth.edu (Gregory W. Froehlich) wrote:
>
>> In article <1994Oct28.165932.3706@emba.uvm.edu>
>> gdavis@griffin.emba.uvm.edu (Gary Davis) writes:
>> 
>> > Does anyone have any further information on this potentially catastrophic
>> > problem?
>> > 
>> 
>> I'd start by asking myself if I had any reason to think that population
>> statistics on prevalence of testicular cancer, etc. were collected any
>> differently today than 50 years ago. (Almost certainly).
>> 
>> Then I'd ask whether the diagnostic methods for testicular carcinoma
>> are different now than 50 years ago (They are).
>> 
>> Then I'd ask, how might these differences cloud my perception of what's
>> going on? (And then try to take those biases into account).
>> 
>> ------------------
>> Greg Froehlich, MD
>> White River Junction, VT
>
>I'll second those, good suggestions all.  Comparisons of disease incidence
>over time are fraught with methodological peril.  That understood, the
>leading hypothesis IF the effect is real is dioxins.  It turns out they
>have estrogenic effects in extremely tiny concentrations, and they're
>byproducts of a wide variety of manufacturing processes.  Their effect
>apparently occurs during critical stages of embryological development.
>

Although the "environmental justice" folks may wrinkle their brows at
the news, we need to consider that:

          Testicular Cancer Incidence (cases per 100,000 per yr)

             1973-74            1987-88

Whites         3.3                4.7 
Blacks         0.9                0.7

These data would cast some doubt on an environmental etiology.  If the
cause were related to the environment, it would follow that white males
were being placed at higher risk than black males.  That hypothesis is,
of course, at odds with the currently fashionable idea that minority
communities are being selectively targetted by polluting industries.

----------------------------------------------
Data from:  NIH 91-2789






From dougb@comm.mot.com  Mon Nov  7 20:44:58 EST 1994
Article: 87056 of sci.med
Newsgroups: sci.med
Path: bigblue.oit.unc.edu!concert!gatech!howland.reston.ans.net!math.ohio-state.edu!news3.acns.nwu.edu!ftpbox!mothost!lmpsbbs!sc736!dougb
From: dougb@sc736 (Doug Bank)
Subject: Re: Why is testicular cancer increasing?
Reply-To: dougb@comm.mot.com 
Organization: Motorola Land Mobile Products Sector
Date: Tue, 1 Nov 1994 19:30:57 GMT
Message-ID: <1994Nov1.193057.8476@lmpsbbs.comm.mot.com>
References:  <1994Oct28.165932.3706@emba.uvm.edu>
Sender: news@lmpsbbs.comm.mot.com (Net News)
Nntp-Posting-Host: 145.1.146.194
Lines: 148

In article <1994Oct28.165932.3706@emba.uvm.edu>, gdavis@griffin.emba.uvm.edu (Gary Davis) writes:
> 
>  I've seen two very informative television documentaries concerning the 
> apparent increase in male testicular cancer, which formally was not only
> rare, but was confined to a few men who had undescended testicle, usually
> not in the inguinal canal, but in the abdomem.

Speaking as someone who has had this cancer, where did you see these
documentaries?  Any names or channels?

> Does anyone have any further information on this potentially catastrophic
> problem?

Here is an article you may find helpful:

                  Copyright 1993 Sentinel Communications Co.
                              THE ORLANDO SENTINEL

                        October 10, 1993 Sunday, 3 STAR

Headline: Studies Find Toxic Link To Breast Cancer;
Doctors Now Suspect That Chemicals May Be Responsible For
One-Third Of The Cases Reported In The United States.

BYLINE: By Delthia Ricks of The Sentinel Staff

   The search for breast cancer's cause has been one futile quest after
another.

   Despite decades of study, dietary  fat  doesn't seem to cause it. Heredity
plays only a small role. Even an esoteric investigation of women's whorly
fingerprint patterns a decade ago didn't pan out.

   Now there's evidence of a link in the food you eat, the tap water you drink
and the yard you spray for bugs and weeds.

   Growing numbers of breast-cancer scientists suspect that the chemicals used
in agriculture, industry and lawn care may be responsible for as much as
one-third of all the breast cancer in the United States today.

   Environmental poisons have long been linked to cancer, but usually to
leukemia, lymphoma and relatively rare tumors.

   Recent studies suggest, however, that a large family of chemicals -
especially a group known as organochlorine pesticides - may also play a role in
triggering breast cancer, the most common type of cancer in women.

   The studies have found that the chemicals don't simply kill tissue - they may
also masquerade as the female hormone estrogen and linger in the body, setting
the stage for  cancer.

   The chemicals first infiltrated our ground water and food chain decades ago;
while some have been banned, they can remain active in the environment for
years.

   Increasingly sophisticated tests are allowing doctors to identify the
chemicals in breast tumors and pre-cancerous cysts:

   Last year, doctors retrieved the makings of a miniature toxic dump from the
breast tumors of 20 women. The joint study by  cancer  specialists in Michigan
and Connecticut found traces of DDT, an organochlorine banned in 1973; DDT's
breakdown product, DDE; Dieldrin, another pesticide limited by federal law to
nonagriculturual uses; and polychlorinated biphenyls - PCBs - the electrical
insulator banned in 1978.

   Earlier this year, Dr. Mary Wolff, an epidemiologist at Mount Sinai School of
Medicine in New York, reported in the Journal of the National Cancer Institute
that DDE was the primary poison in blood samples taken from women who later
developed breast cancer.  Wolff concluded that women with high blood levels of
DDE are up to four times as likely to develop breast  cancer  as those without
the poison in their blood.

   Two months ago, researchers at Columbia University found organochlorine
pesticides in breast cysts removed from patients at New York's Presbyterian
Medical Center.

   Such discoveries have set the scientific community astir because they could
explain the vast number of breast  cancers  that have no direct link to heredity
or known risk factors such as obesity or alcoholism.

   "The reason we're pursuing this is because it makes a lot of sense," said Dr.
Devra Davis, a toxicologist at the U.S. Department of Health and Human Services
in Washington. "It ties a lot of things together, and allows us to link a lot of
information that had been unrelated. The evidence supporting all of this gets
stronger every day."

   Dr. Rebecca Moroose, an Orlando oncologist, believes researchers may be on
the trail of a significant breast- cancer  risk.

   "I think this definitely is entitled to a lot of investigation," she said.
"But I also think there will not be just one answer to the breast  cancer
dilemma. This could be a co-factor. There may be a number of factors that
interact, such as a genetic predisposition and environmental stimulation - and a
hormone change."

   Estrogen, produced by the ovaries, is responsible for the development of
female sex characteristics; it regulates the menstrual cycle and stimulates the
thickening of the uterine lining.                                               

   Estrogen's three forms - estrone, estradiol and estriol - all have affinities
for cells in the reproductive tract, the breasts and the brain.  There they
hitch themselves to cells at sites called receptors, much as a key fits a lock
to open a door.

   The problem is, toxins with similar chemical characteristics can act like
passkeys and fit the same locks.

   These "xeno-estrogens" may cruise the bloodstream, lodge in breast tissue and
unlock cells, causing them to multiply and become cancerous. Researchers
speculate that the same xeno-estrogens may also play a role in ovarian cancer
as well as in prostate and testicular cancer in men.

   Atrazine, one of the most widely used pesticides in U.S. farming, and
heptachlor, another organochlorine, appear to have estrogenic effects, Davis
said.

   Scientists have suspected for years that natural estrogen can lead to
cancer under certain circumstances, though they're still not sure how. Working
with poisons, Davis said, may solve two mysteries at once - how xeno-estrogens
cause cancer, and how that process mimics estrogen when the natural hormone
goes awry.

   Statistics show that the number of breast cancer cases diagnosed each year
has more than doubled since 1973. And epidemiologists say that's just part of a
larger upward trend that began in the United States, Canada and Western Europe
in the early 1930s.

   According to the American  Cancer  Society, an estimated 11,300 Florida women
will develop breast cancer this year, compared with 6,600 new cases reported
in 1986.

   No pesticide has yet been banned because of a supposed link to breast
cancer.  Atrazine, an organochlorine suspected of estrogenic effects, is used
widely on sugar-cane fields in South Florida. And homeowners statewide apply a
range of toxic compounds to their lawns and gardens.

   "The preliminary studies in breast cancer show that such chemicals may
influence breast-cell multiplication," said Dr. Clark Heath, vice president
for epidemiology at the American Cancer Society's headquarters in Atlanta.

   "But answering these questions definitively will be a matter of a lot of
basic research," he added. "It's a very complicated area."

-- 
Doug Bank                       Secure Design Center
dougb@ecs.comm.mot.com          Motorola Communications Sector
dougb@nwu.edu                   Schaumburg, Illinois
dougb@casbah.acns.nwu.edu       708-576-8207                    


From kellmeye@ux1.cso.uiuc.edu Mon Nov  7 20:45:55 EST 1994
Article: 87106 of sci.med
Path: bigblue.oit.unc.edu!concert!inxs.ncren.net!taco.cc.ncsu.edu!gatech!howland.reston.ans.net!vixen.cso.uiuc.edu!ux1.cso.uiuc.edu!kellmeye
From: kellmeye@ux1.cso.uiuc.edu (kellmeyer steven l)
Newsgroups: sci.med
Subject: Re: Why is testicular cancer increasing?
Date: 2 Nov 1994 16:16:38 GMT
Organization: University of Illinois at Urbana
Lines: 45
Message-ID: <398e16$8hn@vixen.cso.uiuc.edu>
References: <1994Oct28.165932.3706@emba.uvm.edu> <38stfh$knp@glock.ramp.com>
NNTP-Posting-Host: ux1.cso.uiuc.edu

massimin@glock.ramp.com (Esther Massimini) writes:

>Gary Davis (gdavis@griffin.emba.uvm.edu) wrote:

>: hypospadias are common!
>The PDR lists hypospadias as a possible side effect if one becomes
>pregnant while on (or within 3 months of stopping) the pill. In parenting
>forums I have seen several mothers posting on this as well...

>: The documentaries concentrated on studies showing such problems not only
>: among humans, but also fish and alligators and so forth.
>: It also estimated male fertility to be about 50 % of what it was 100 years
>: ago. In other words men on average produce fewer sperm and more deformed
>: sperm than 100 years ago.

>: The answers seem elusive, however some chemical that simulates estrogen
>: in the environment is thought responsible.

>It's the environment IMHO.  Look at the increase in breast cancers. I
>think eventually these will all be shown to have a common root....

According to the front page article in my paper last week, a woman's chances
of getting breast cancer increase by 50% if she's had an abortion. One may
argue whether there is a common root between this and the use of the pill.
I realize that everyone will immediately say that the study was not 
conclusive, even one of the author's said not to allow it to influence your
decisions until it's been replicated, etc.  I will only note that it's 
unusual for the press to add these qualifications to any study which shows
an increase of 50% in the risk for breast cancer. They generally just go
hog-wild predicting the end of the world as we know it. As I recall, silicone
breast implants were taken off the market for a much less clear link. 
Isn't it odd that no one is pushing for abortion to be taken off the market?
I'm sure someone will count this as moralizing, but I would really like to
know why silicone doesn't enjoy the same protection abortion does.

>-- 
>Esther M. Massimini		   --  massimin@ramp.com   
>(Mommy to Amanda Christine 6/29/88 OR  				
>and Armand James 2/7/90)           --  massimin@saifr00.ateng.az.honeywell.com

Steve	    
-- 
Steve Kellmeyer             kellmeye@ux1.cso.uiuc.edu
"It is a very great poverty to decide that a child must die 
that you may live as you wish"           --Mother Theresa 


From russ@pmafire.inel.gov Mon Nov  7 20:47:09 EST 1994
Article: 87226 of sci.med
Newsgroups: sci.med
Path: bigblue.oit.unc.edu!concert!gatech!howland.reston.ans.net!news.sprintlink.net!EU.net!uunet!pmafire!russ
From: russ@pmafire.inel.gov (Russ Brown)
Subject: Re: Why is testicular cancer increasing?
Message-ID: <1994Nov2.180824.9391@pmafire.inel.gov>
Date: Wed, 2 Nov 94 18:08:24 GMT
References: <1994Oct28.165932.3706@emba.uvm.edu> <38stfh$knp@glock.ramp.com> <398e16$8hn@vixen.cso.uiuc.edu>
Organization: WINCO
Lines: 43

In article <398e16$8hn@vixen.cso.uiuc.edu>,
kellmeyer steven l <kellmeye@ux1.cso.uiuc.edu> wrote:
>massimin@glock.ramp.com (Esther Massimini) writes:
>
>>Gary Davis (gdavis@griffin.emba.uvm.edu) wrote:
>
>>: hypospadias are common!
>>The PDR lists hypospadias as a possible side effect if one becomes
>>pregnant while on (or within 3 months of stopping) the pill. In parenting
>>forums I have seen several mothers posting on this as well...
>
>>: The documentaries concentrated on studies showing such problems not only
>>: among humans, but also fish and alligators and so forth.
>>: It also estimated male fertility to be about 50 % of what it was 100 years
>>: ago. In other words men on average produce fewer sperm and more deformed
>>: sperm than 100 years ago.
>
>>: The answers seem elusive, however some chemical that simulates estrogen
>>: in the environment is thought responsible.
>
>>It's the environment IMHO.  Look at the increase in breast cancers. I
>>think eventually these will all be shown to have a common root....
>
>According to the front page article in my paper last week, a woman's chances
>of getting breast cancer increase by 50% if she's had an abortion. One may
>argue whether there is a common root between this and the use of the pill.
>I realize that everyone will immediately say that the study was not 
>conclusive, even one of the author's said not to allow it to influence your
>decisions until it's been replicated, etc.  I will only note that it's 
>unusual for the press to add these qualifications to any study which shows
>an increase of 50% in the risk for breast cancer. They generally just go
>hog-wild predicting the end of the world as we know it. As I recall, silicone
>breast implants were taken off the market for a much less clear link. 
>Isn't it odd that no one is pushing for abortion to be taken off the market?
>I'm sure someone will count this as moralizing, but I would really like to
>know why silicone doesn't enjoy the same protection abortion does.
>
For women under 45, the reported increase in risk  was from 0.1% to 0.15%. 
The media did not report the confidence range or the number of cases used to
develop the "50%" increase.





From montague@world.std.com Mon Nov  7 21:15:00 EST 1994
Article: 87157 of sci.med
Newsgroups: sci.environment,talk.environment,sci.med
Path: bigblue.oit.unc.edu!concert!inxs.ncren.net!taco.cc.ncsu.edu!gatech!howland.reston.ans.net!news.moneng.mei.com!uwm.edu!lll-winken.llnl.gov!decwrl!pa.dec.com!world.std.com!montague
From: montague@world.std.com (Peter Montague)
Message-ID: <199411022159.AA27116@world.std.com>
Subject: RACHEL: Potent Immune Poison
Date: Wed, 2 Nov 1994 16:59:01 -0500
X-Received: by usenet.pa.dec.com; id AA18557; Wed, 2 Nov 94 14:08:04 -0800
X-Received: by pobox1.pa.dec.com; id AA14743; Wed, 2 Nov 94 14:08:02 -0800
X-Received: from ftp.std.com by inet-gw-3.pa.dec.com (5.65/10Aug94)
	id AA24082; Wed, 2 Nov 94 14:04:37 -0800
X-Received: from world.std.com by ftp.std.com (8.6.8.1/Spike-8-1.0)
	id QAA07513; Wed, 2 Nov 1994 16:58:57 -0500
X-Received: by world.std.com (5.65c/Spike-2.0)
	id AA27116; Wed, 2 Nov 1994 16:59:01 -0500
X-To: erf@igc.apc.org
Lines: 244
Xref: bigblue.oit.unc.edu sci.environment:45231 talk.environment:18983 sci.med:87157

=======================Electronic Edition========================

            RACHEL'S ENVIRONMENT & HEALTH WEEKLY #414
                     ---November 3, 1994---
                           HEADLINES:
               POTENT IMMUNE SYSTEM POISON: DIOXIN
                           ==========
                Environmental Research Foundation
               P.O. Box 5036, Annapolis, MD  21403
          Fax (410) 263-8944; Internet: erf@igc.apc.org
                           ==========
          Back issues available via anonymous ftp from
      ftp.std.com/periodicals/rachel and via gopher server
   at gopher.std.com and at envirolink.org and at igc.apc.org.
=================================================================

POTENT IMMUNE SYSTEM POISON: DIOXIN

The immune system is a complex set of specialized cells and
organs that defends the body against attack by "foreign"
invaders.  When it functions properly, the immune system fights
off diseases caused by bacteria, viruses, fungi, parasites, and
cancer cells.  "When it malfunctions, however, it can unleash a
torrent of diseases, from allergy to arthritis to cancer to
AIDS," according to the federal National Institutes of Health
(NIH).[1]

At the heart of the immune system is the ability to distinguish
between self and nonself.  A healthy immune system protects the
"self" and attacks only the "nonself."  Virtually every cell in
your body carries distinctive molecules that identify it as self.
Cells lacking a "self" marker are quickly perceived as
"foreign," attacked, and eliminated by the immune system.

The National Institutes of Health (NIH) describes the immune
system this way: "The immune system, which equals in complexity
the intricacies of the brain and nervous system, displays several
remarkable characteristics.  It can distinguish between self and
nonself.  It is able to remember previous experiences and react
accordingly: once you have had chicken pox, your immune system
will prevent you from getting it again.  The immune system
displays both enormous diversity and extraordinary specificity:
not only is it able to recognize many millions of distinctive
nonself molecules, it can produce molecules and cells to match up
with and counteract each one of them.  And it has at its command
a sophisticated array of weapons.

"The success of this system in defending the body relies on an
incredibly elaborate and dynamic regulatory-communications
network. Millions and millions of cells, organized into sets and
subsets, pass information back and forth like clouds of bees
swarming around a hive. The result is a sensitive system of
checks and balances that produces an immune response that is
prompt, appropriate, effective, and self-limiting."[1]

The immune system can fail in two ways: if it is damaged, it can
fail to attack foreign invaders, and can thus allow infections or
cancers to develop.  On the other hand, if the immune system
fails to distinguish self from nonself, it can overreact and
attack the self, causing "autoimmune" diseases such as arthritis,
asthma, lupus, or Type I diabetes (insulin-dependent diabetes
mellitus).  Other autoimmune diseases include scleroderma,
Graves' disease, Addison's disease, Hashimoto's disease,
myasthenia gravis, lymphocytic adenohypophysitis (also called
Sheehan's syndrome), mucocutaneous candidiasis, Schmidt's
syndrome, and autoimmune thyroid disease.

Dioxin: Potent Immune System Poison

U.S. Environmental Protection Agency's (EPA's) 1994 draft
reassessment of dioxin emphasized that dioxin damages the immune
system directly and indirectly.  From studies of rats, mice,
guinea pigs, rabbits, cattle, marmosets, monkeys, and humans, EPA
concludes that even low doses of dioxin attack the immune system.
Dioxin directly reduces the number of B cells (immune cells that
develop in the bone marrow, then circulate throughout the blood
and lymph, fighting off invaders).  And it reduces the number of
T cells (immune cells that develop in the thymus, then circulate
throughout the body, attacking invaders), but dioxin's attack on
T cells seems to be indirect.  EPA says, "One potentially
important indirect mechanism is via effects on the endocrine
system.  Several endocrine hormones have been shown to regulate
immune responses, including glucocorticoids, sex steroids,
thyroxine, growth hormone, and prolactin. Importantly, TCDD
[dioxin] and other related compounds have been shown to alter the
activity of these hormones."[2,pg.9-49]

EPA goes on to say, "It is important to consider that if an acute
exposure to TCDD even temporarily raises the TCDD body burden at
the time when an immune response is initiated, there may be a
risk of adverse impacts even though the total body burden may
indicate a relatively low average TCDD level."  In other words, a
single dose of dioxin at the wrong time may damage your immune
system's ability to protect you.

EPA then says, "Furthermore, because TCDD alters the normal
differentiation of immune system cells, the human embryo may be
very susceptible to long-term impairment of immune function from
in utero [in the womb] effects of TCDD on developing immune
tissue."  In other words, dioxin can prevent the immune system
>from  developing properly in an unborn child, with lifelong
consequences, EPA believes.  "Animal studies suggest that some
immunotoxic responses may be evoked at very low levels of dioxin
exposure," EPA says.[2,pg.9-50]

Linda Birnbaum, director of research at the U.S. EPA Health
Effects Laboratory in Research Triangle Park, N.C., was the
leader of EPA scientific team reassessing dioxin.  She says,
"Dioxin appears to be a carcinogen in fish, rodents, and other
mammals, including humans.  But dioxin can also modulate [modify]
the immune system resulting in an inability to fight disease.  It
is a very powerful immunosuppressant. But it can also upregulate
[excite] the immune system so that you start becoming
hypersensitive, developing autoimmunity and allergies. Depending
upon the stage [of growth] of the animal and the species,
sometimes you observe immunosuppression and in other cases you
observe upregulation."[3,pg.4]

Birnbaum goes on to describe Taiwanese children, exposed to
dioxin-like chemicals, who had unusually frequent respiratory
infections and ear infections (otitis).  Further, she described
an Inuit population in Quebec with elevated levels of dioxin in
their bodies from eating the fat of marine mammals (seals); their
children have "very high incidences of respiratory infections and
otitis [ear infections], and also a very decreased take of
vaccinations," Birnbaum says.[3],pg.11 In other words,
vaccinations don't work well in these children, perhaps because
their immune systems have been damaged.

Birnbaum says there is no threshold for immunotoxic responses to
dioxin;[3,pg.14] in other words, there is no level of dioxin
below which the immune system is not affected.  Put another way:
any amount of dioxin seems to do some damage to the immune
system, at least in animals; there is no "safe" dose.

In laboratory mice, a single tiny dose of dioxin causes increased
deaths when the mice are challenged with an influenza virus.[4]
It is worth emphasizing that the effective dose of dioxin is very
small: 10 nanograms of dioxin per kilogram of bodyweight (10
ng/kg) harms the mouse immune system enough to increase the death
rate from influenza virus.  To get 10 ng/kg into perspective,
consider that a single 5-grain aspirin tablet taken by a
150-pound adult is a dose of 4.7 MILLION nanograms of aspirin per
kilogram of bodyweight (4,761,936 ng/kg).  For an adult human to
get a dose of aspirin equivalent to the dose of dioxin that harms
the mouse immune system, you would have to divide a single
aspirin tablet into 470,000 pieces (nearly half a million pieces)
and eat only one piece.  Is the human immune system as sensitive
to dioxin as the mouse's?  No one yet knows.

What about animals more human-like than mice?  Tom Webster of the
Boston University School of Public Health cites evidence that the
number of immune cells in rhesus monkeys is changed by a dioxin
body burden of 270 ng/kg; in marmosets, the number of immune
cells is changed at only 6 to 8 ng/kg of dioxin.  "While the
medical implications of this effect are unknown, it appears to
occur at about the average human body burden of dioxin-like
compounds," he says.  In other words, average residents of North
America carry 7 to 9 ng/kg in their bodies now, and 6 to 8 ng/kg
alters the immune systems of marmosets.[4,pg.8]   "Similar
effects [immune cell alterations] were seen in the children of
mothers who lived in dioxin-contaminated Times Beach, Missouri
during and after pregnancy," Webster notes, citing work by Gerson
Smoger and others.[4,pg.7]

This past summer, German researchers published a study of the
health of 158 chemical workers who had been exposed to dioxin in
1953 during an industrial accident at a BASF chemical plant.[5]
The 158 exposed workers were compared to 161 unexposed workers.
The dioxin-exposed workers experienced more frequent infections
and parasitic diseases during the 36 years after exposure,
consistent with immune system damage.  Especially noticeable were
increases in respiratory infections, thyroid diseases, disorders
of the peripheral nervous system, and appendicitis.  Mental
disorders were also increased.  All together, the highly-exposed
group had 18% more recorded episodes of illness than the control
group.

Ironically, the largest source of dioxin entering the environment
today is medical incinerators.  Together, medical incinerators
and municipal solid waste (msw) incinerators account for 95% of
all dioxin emissions into the air of the U.S., according to U.S.
EPA.[6,pg.2]  The good news is: these technologies are not needed
and could be phased out rapidly, if public health authorities
began to take their DISEASE PREVENTION responsibilities
seriously.  Plans for new incinerators could be easily abandoned.
For both medical wastes and municipal wastes, alternatives
already exist that are cleaner, safer, and less expensive.  (The
chief appeal of incinerators is political: massive campaign
contributions by the waste industry.)

Unfortunately, instead of planning to phase out incinerators, EPA
has announced plans to "regulate" incinerator emissions more
tightly by requiring air pollution scrubbers.  Scrubbers will not
decrease dioxin production, but will move dioxin from the air
emissions into the incinerator ash, which gets buried in shallow
pits in the ground. Thus, current public health policies are
creating a legacy of unpleasant surprises for our children.
                                                --Peter Montague
===============
[1] Lydia Woods Schindler, UNDERSTANDING THE IMMUNE SYSTEM [NIH
Publication No. 88-529] (Bethesda, Md.: National Institutes of
Health, July, 1988), pg. 1.

[2] U.S. Environmental Protection Agency, HEALTH ASSESSMENT
DOCUMENT FOR 2,3,7,8-TETRACHLORODIBENZO-p-DIOXIN (TCDD) AND
RELATED COMPOUNDS. VOL. III OF III. [EPA/600/BP-92/001c]
(Cincinnati, Ohio: U.S. Environmental Protection Agency, August,
1994.)  This is the official draft of "Chapter 9" of the EPA
dioxin reassessment, also known as the "risk characterization
chapter." Available free while supplies last; telephone (513)
569-7562 in Cincinnati.

[3] Linda Birnbaum, GREAT LAKES WATER QUALITY BOARD 102ND
MEETING, CHICAGO, ILLINOIS, JULY 15, 1993, PRESENTATION BY LINDA
BIRNBAUM, U.S. EPA (Washington, D.C.: International Joint
Commission, Great Lakes Water Quality Board, Dec. 21, 1993), pg.
4.  Available from us for $4.00.

[4] Tom Webster, DIOXIN AND HUMAN HEALTH: A PUBLIC HEALTH
ASSESSMENT OF DIOXIN EXPOSURE IN CANADA (Boston: Boston
University School of Public Health, 1994), pg. 7, citing
unpublished work by Linda Birnbaum and others.  Available from us
for $4.00.

[5] Andreas Zober and others, "Morbidity follow up study of BASF
employees exposed to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)
after a 1953 chemical reactor incident," OCCUPATIONAL AND
ENVIRONMENTAL MEDICINE Vol. 51, No. 7 (July 1994), pgs. 479-486.

[6] Lynn Goldman, STATEMENT OF LYNN GOLDMAN, M.D., ASSISTANT
ADMINISTRATOR FOR PREVENTION, PESTICIDES AND TOXICS, U.S.
ENVIRONMENTAL PROTECTION AGENCY, SEPTEMBER 13, 1994 (Washington,
D.C.: U.S. Environmental Protection Agency, September 13, 1994).

Descriptor terms:  immune system; morbidity; nih; national
institutes of health; dioxin; incineration; taiwan; children;
bronshitis; upper respiratory infections; basf; occupational;
safety and health; times beach; mo; tom webster; linda birnbaum;
gerson smoger; epa; us environmental protection agency; germany;
thyroid; appendix; appendicitis; peripheral neuropathy; mental
health; medical waste; infectious waste; msw; municipal solid
waste; corruption; elections; campaign reform; campaign
contributions;


