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#879 -- Basic Principles, 02-Nov-2006


Rachel's Democracy & Health News #879

"Environment, health, jobs and justice--Who gets to decide?"

Thursday, November 2, 2006..............Printer-friendly version
www.rachel.org -- To make a secure donation, click here.

Featured stories in this issue...

What Guides Our Work?
  What are we doing and why are we doing it? Are we succeeding?
Harmful Chemicals May Leach from Septic Systems
  Septic systems do not effectively remove hormone-disrupting
  chemicals, which can leach into groundwater.
Breast Cancer and Environmental Exposure To Traffic Fumes
  A study links breast cancer to pollutants from automobile traffic,
  specifically polycyclic aromatic hydrocarbons (PAHs).
Fertile Grounds for Inquiry
  Are chemicals interfering with human reproduction? Approximately
  12% of American couples experienced impaired fecundity in 2002. This
  is a 20% increase from the 6.1 million couples who reported an
  inability to have children in 1995.
White Privilege: Swimming in Racial Preference
  Without meaning to offend anyone, it seems like a good idea to
  unpack the true history of the U.S. Our institutions were created by
  Europeans who viewed it as their sacred obligation to dominate the
  "lesser races," meaning all non-whites. As a result, white people
  today enjoy unearned privilege and power that they may not even


From: Rachel's Democracy & Health News #879, Nov. 2, 2006
[Printer-friendly version]


By Peter Montague

Occasionally a reader will ask, "What guides your selection of stories
for Rachel's News?" In this short series, we'll provide an answer.

Basically, the question is, What are we doing and why are we doing it?
Are we succeeding?

Here at Rachel's News we hold a fundamentally conservative view of our
role: this world came to us as gift from our forebears and we have an
obligation to pass it along undiminished and undamaged.

Simple ideas guide our work

Our work springs from a simple, universal ethic -- every culture and
every religion endorses the Golden Rule [1,2], which says, "Treat
others the way you want to be treated." This tells us, first, to
alleviate suffering. This, in turn, leads directly to human rights --
we all have a basic right to a life free of suffering, to the extent
possible. The elements of such a life were laid out in the Universal
Declaration of Human Rights, which the U.S. endorsed Dec. 10, 1948.


For us, the Golden Rule and the Universal Declaration together define
justice. Justice is that which tends to manifest the Golden Rule and
the Universal Declaration; injustice tends to manifest the opposite.
It is unjust -- unfair and therefore unacceptable -- to impose
suffering on others or to stand by and allow suffering to go unnoticed
or unchecked. It is unjust -- unfair and unacceptable -- to deprive
anyone of any human right as spelled out in 1948.

In recent years, science has confirmed what people have always known:
human community is essential for human well-being. We humans evolved
as social creatures[3,4] who cannot thrive when separated from our
circle of family, friends, acquaintances, and animal companions.
Social isolation makes us sick and leads to an early death. This
is one reason why racism[5] and white privilege are profoundly
wrong. At a minimum, they create social isolation, which leads to
illness and suffering, and so they are unjust and unacceptable.

Furthermore, when we damage nature we diminish our own -- and
everyone's -- possibilities for a life as free as possible of
suffering. When we create havoc via global warming or damage to the
Earth's protective ozone layer, or when we pave over fertile farmland,
or exterminate the fish of the sea or the birds of the air, we
diminish everyone's possibilities for securing life, liberty and the
pursuit of happiness (to quote the Declaration of Independence of
1776). To us, this is unjust and unacceptable.

Our dependence of all creatures

Science now confirms the wisdom of indigenous peoples, that we are all
interdependent, all humans, all species. We humans are part of, and
are supported by, a biological platform of enormous complexity, which
we cannot understand, but which we know with absolute certainty
nourishes and sustains us. Even a child can see that, without it. we
are lost.

Because human rights and justice cannot be secured if our biological
platform is shredded, we all have a right to intact natural and social
environments -- environments that enable us to provide for ourselves
the essentials of air, water, food, shelter and community (the basic
prerequisites for "happiness"), which we all require to prevent

Furthermore, as Jeremy Bentham articulated in 1789, animals too have
a right to live a life free of suffering to the extent possible. As
Bentham said, the question is not whether they can reason, or whether
they can talk. Their right to live free from torment hinges on the
question, can they suffer? Their suffering stands on a moral plane
with ours.

Because the biological platform, upon which we all depend, cannot be
secured unless we are free to take action to protect it, human rights
and justice are essential requirements for human survival.

The earth is our home and we have to take care of it, for the reason
that we absolutely depend on it. To preserve our home without
understanding all its billions of inter-related parts, we can aim to
preserve every part of it. No part of creation can be presumed
dispensable. We can say we know what's dispensable, but what if we're
wrong? In recent years we came close to making the surface of the
earth uninhabitable for humans because we failed to understand how
DuPont's CFC chemicals were damaging the ozone layer. It was a close
call. Our ignorance is vast. As Albert Einstein reportedly said, "We
still do not know one-thousandth of one percent of what nature has
revealed to us."[6]

When flying blind, go cautiously

Whenever we set out to do anything that might harm any part of our
home, we can move slowly, move cautiously, as we would when flying
blind. Like any good pilot, we can constantly check for signs of
trouble, and when any such signs are observed, we can take action to
prevent further trouble. This is common sense and ancient wisdom. Look
before you leap. A stitch in time saves nine. Prevention is better
than cure, Erasmus told us.

We are all in this boat together and none of us has the right to
endanger the ship. To do so is a deep and intolerable injustice to

Purpose of Government

From these principles, we understand the purpose of government. For
example, the Declaration of Independence of 1776 tells us,

"We hold these truths to be self-evident, that all men are created
equal, that they are endowed by their Creator with certain unalienable
Rights, that among these are Life, Liberty and the pursuit of
Happiness. That to secure these rights, Governments are instituted
among Men, deriving their just powers from the consent of the

The purpose of government, then, is to secure human rights, including
the right to enjoy intact natural and social environments without
which we cannot have life, liberty or the pursuit of happiness. Put
another way, the purpose of government is to protect and secure the
things that we all depend upon and share in common, the air, water,
soil, human language and accumulated knowledge, the genome, public
health, reciprocal relationships of trust, and much more.

And finally any government becomes illegitimate when it fails to gain
the consent of the governed. People have an inherent, unalienable
right to participate in the decisions that affect their lives.

These, then, are the basic, conservative ideas that guide our choice
of stories for Rachel's news. Now the plot thickens. More next time.


[3] As CrossRoadsMinistry.org says, racism is one group's individual
race prejudice enforced by the misuse of power via systems and

[5] A shorthand version of the Universal Declaration is Franklin
Roosevelt's "four freedoms," which he described this way: "In the
future days which we seek to make secure, we look forward to a world
founded upon four essential human freedoms. The first is freedom of
speech and expression -- everywhere in the world. The second is
freedom of every person to worship God in his own way -- everywhere in
the world. The third is freedom from want, which, translated into
world terms, means economic understandings which will secure to every
nation a healthy peacetime life for its inhabitants -- everywhere in
the world. The fourth is freedom from fear, which, translated into
world terms, means a world-wide reduction of armaments to such a point
and in such a thorough fashion that no nation will be in a position to
commit an act of physical aggression against any neighbor -- anywhere
in the world. That is no vision of a distant millennium, it is a
definite basis for a world attainable in our own time and generation.
That kind of world is the very antithesis of the so called 'new order'
of tyranny which the dictators seek to create with the crash of a
bomb. To that new order we oppose the greater conception -- the moral
order. A good society is able to face schemes of world domination and
foreign revolutions alike without fear.... Freedom means the supremacy
of human rights everywhere. Our support goes to those who struggle to
gain those rights and keep them."

[6] Einstein quoted in The Sun (June 2006), pg. 48.

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From: Reuters Health, Aug. 15, 2006
[Printer-friendly version]


By Megan Rauscher

NEW YORK (Reuters Health) -- Septic systems may not remove natural
hormone-disrupting chemicals -- like estrogen excreted in women's
urine -- from wastewater before it gets into groundwater, which feeds
many drinking water supplies, according to tests conducted in Cape
Cod, Massachusetts.

In Cape Cod, more than 85 percent of residential and commercial
properties use septic systems.

In a telephone interview, Dr. Chris Swartz said: "We did find both
natural estrogen and alkyl phenols from detergents entering
groundwater at concentrations very similar to concentrations that have
been documented in the literature to show adverse reproductive effects
in fish swimming in rivers downstream of wastewater treatment

Other chemicals detected in groundwater near the tested septic system
include caffeine and detergent brightening compounds.

Swartz, senior scientist at the Silent Spring Institute in Newton,
Massachusetts, said there is still "hot debate" in the Environmental
Protection Agency and among scientists in general as to whether the
concentrations of these and other chemicals that are being found in
the environment have human health implications.

"The biggest concern is for prenatal exposures, because fetuses are
exquisitely sensitive to any type of hormonal imbalances during their
development," he explained.

Swartz hopes publication of his team's findings in the August 15 issue
of Environmental Science and Technology will fuel dialogue among land
use planners and policy makers about what septic systems are and are
not removing.

"It's important to understand this if we are going to rely on septic
systems," said Swartz.

Currently about 25 percent of US households and probably a larger
amount globally, Swartz noted, use on-site septic systems for
household waste treatment as opposed to public sewage treatment

"And there is a US and global trend toward decentralized wastewater
treatment," Swartz said.

Prior research on septic systems have dealt only with nutrients such
as nitrogen and phosphorus that may leach from septic tanks, get into
groundwater, and eventually make it to surface body waters that the
groundwater feeds.

The current tests, Swartz said, clearly show that other chemicals,
like natural estrogens, known to interfere with human hormonal
regulation, are also getting away from septic system treatment. Future
studies, he concludes, are needed to determine the extent and
potential effects of drinking water contamination with hormone-
disrupting chemicals and other potentially harmful chemicals.

SOURCE: Environmental and Science Technology August 15, 2006.

Reuters Health

Copyright 1995-2006 Medicine Online Inc.

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From: American Association for Cancer Research, Jun. 1, 2005
[Printer-friendly version]


By Jing Nie, Jan Beyea, Matthew Bonner, Daikwon Han, John Vena,

Peter Rogerson, Dominica Vito, Paola Muti, Maurizio Trevisan and Jo

Polycyclic aromatic hydrocarbons (PAHs) are an important component of
air pollution and potential human carcinogens. While they have been
shown to cause mammary cancer in animal studies, the association
between PAH exposure and breast cancer risk is not well understood.

Traffic emissions are one of the major sources of PAH exposure in
cities. Further, growing evidence suggests that there may be critical
time periods of exposure in breast cancer initiation and development.

In this study, we examined the association between breast cancer risk
and exposure to PAHs from traffic emissions estimated for each woman
at menarche, at the time when she had her first pregnancy and birth,
and at 20 and 10 years prior to interview, using data collected from
the Western New York Exposures and Breast Cancer (WEB) study, a
population based case control study in western New York.

All participants were women, aged 35-79, residents of Erie and Niagara
Counties. Cases had incident, primary, histologically-confirmed breast
cancer. Controls were randomly selected and frequency-matched to cases
on age, race and county. In-person interviews were used to collect
data on potential breast cancer risk factors including self-reported
lifetime residential history. Traffic volumes on roads were obtained
from historical records for the years from 1960-2002. Tailpipe
emission data were based on previous reports, including measurements
carried out in tunnels or on individual vehicles run in place on test

A geographic model, developed by Dr. Beyea and colleagues from the
Long Island Breast Cancer project, was used to reconstruct historical
traffic PAHs, using BaP as a surrogate for total PAH exposure. Cruise
emissions, cold engine emissions and intersection emissions were used
to estimate total traffic PAH emissions.

Meteorological information was also utilized in the geographic
dispersion model to assign PAH exposure at each residence. The model
was validated using data collected from both Long Island and our study

We found evidence that higher exposure to traffic PAH emissions at
menarche was associated with increased risk of premenopausal breast
cancer (OR 2.07, 95% CI 0.91-4.72, p for trend 0.03) and emissions at
the time of a woman's first birth was associated with postmenopausal
breast cancer (OR 2.58, 95% CI 1.15-5.83, p for trend 0.19).

Both associations were limited to lifetime non-smokers. There was no
association of traffic emissions with risk for any of the other time

These findings provide evidence for both the potential importance of
early exposures and the potential importance of an environmental agent
in risk of breast cancer.

Copyright 2005 by the American Association for Cancer Research.

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From: Environmental Health Perspectives, Nov. 1, 2006
[Printer-friendly version]


Environmental Effects on Human Reproduction

By Julia R. Barrett

In a world whose population exceeds 6.5 billion, declining human
fertility might not seem to be a critical problem. After all,
overpopulation has been a global concern for decades. Declining
fertility rates in more advanced nations largely reflect the changing
role of women and their rapidly growing presence in the workplace --
fertility declines may stem at least in part from the modern tendency
to delay childbearing until later in life, when fertility naturally

But this doesn't explain the fact that, according to a December 2005
report of the CDC's National Survey on Family Growth (NSFG), the
fastest-growing segment of U.S. women with impaired fecundity (the
capacity to conceive and carry a child to term) is those under 25. The
rising incidence of fertility-impairing health factors such as obesity
also likely plays animportant role. Clues from environmental exposure
assessments, wildlife studies, and animal and human studies hint at
additional factors: exposure to low-level environmental contaminants
such as phthalates, polychlorinated biphenyls (PCBs), dioxins,
pesticides, and other chemicals may be subtly undermining our ability
to reproduce.

As recognized by the American Society of Reproductive Medicine,
infertility is a biological disease that impairs a couple's ability to
achieve a viable pregnancy. It can be caused by hormonal, ovarian,
uterine, urological, and other medical factors. Known risk factors
include advanced age, being over- or underweight, lack of exercise,
smoking, alcohol and substance abuse, sexually transmitted diseases,
and poor nutrition.

According to the American Society of Reproductive Medicine, a medical
infertility cause can be identified, or perhaps only indefinitely
suggested, in approximately 90% of cases and may be multifactorial in
25% of cases. Male factors include low sperm count and sperm
abnormalities, such as altered morphology and low motility. Female
factors stem from ovulation problems such as premature ovarian failure
(early menopause), thyroid irregularities, polycystic ovarian
syndrome, and fallopian tube obstruction.

Up to 10% of infertility cannot be explained medically. Fertility
transcends the reproductive system, notes Louis Guillette, a professor
of zoology at the University of Florida in Gainesville. "When you talk
about infertility, you literally are talking about probably almost
every system in the body -- infertility is an integrated signal of all
these different systems," he explains. "Trying to tease out which
system, or more than likely what multiple systems have been altered,
leading to that phenomenon, is very tough work."

Infertility is generally defined as occurring when a couple cannot
become pregnant after trying to conceive for at least one year (or six
months if the woman is over age 35). According to the 2001 WHO report
Current Practices and Controversies in Assisted Reproduction, at least
80 million people worldwide are estimated to be affected by
infertility. Infertility rates range from less than 5% to greater than
30% depending on location and how infertility is defined, with higher
rates associated with lack of medical care access. Based on the 2005
NSFG report, approximately 12% of American couples experienced
impaired fecundity in 2002. This is a 20% increase from the 6.1
million couples who reported an inability to have children in 1995.

Her side. Female factors in infertility stem from ovulation problems,
thyroid irregularities, polycystic ovarian syndrome, and fallopian
tube obstruction. A trend among women to delay starting a family also
has impacted fertility rates. image: Sebastian Kaulitzki/Shutterstock

Determining whether infertility is actually increasing is more
complicated than these numbers imply, however. In a paper published in
the September 2006 issue of Fertility and Sterility, David Guzick and
Shanna Swan of the University of Rochester School of Medicine and
Dentistry noted that "impaired fecundity" as defined by the NSFG
implies a decrease in fertility, but the same study also showed that
fertility, defined there as a married woman unable to become pregnant
within 12 months, has increased.

The absence of definitive information can frustrate couples
experiencing fertility problems as well as experts. "There seems to be
more to it than can be explained from traditional understanding about
impacts," says Joseph Isaacs, president and CEO of RESOLVE: The
National Infertility Association. "As a patient advocacy group, we
believe more research into environmental impacts is needed. We fear
that future generations may be at risk because of exposures to toxic
substances as early as in utero."

Foundations of Fertility

A person's reproductive potential begins shortly after his or her own
conception. Based on the embryo's chromosomal inheritance, hormonal
signals are created to direct the structure and function of the
reproductive tract. Normal development depends upon a correct balance
of androgen and estrogen signals being delivered at appropriate times.

Fetal development can be altered by external factors as demonstrated
by the human experience with the synthetic estrogen diethylstilbestrol
(DES), prescribed to prevent miscarriage between 1947 and 1971. The
drug didn't affect mothers, and it didn't lower miscarriage incidence;
in fact, it significantly increased it. It also induced changes in the
developing reproductive tract of female offspring.

In the 15 April 1971 issue of the New England Journal of Medicine, it
was reported that daughters with prenatal DES exposure had
significantly increased incidence of vaginal cancer, which is normally
quite rare and was virtually unknown in young women prior to DES.
Later research revealed structural abnormalities of these women's
reproductive tracts and effects in their male offspring including
increased risk of cryptorchidism (undescended testes) and low sperm

The study of endocrine disruptors has raised concerns about the
reproductive effects of exposure to certain environmental compounds
that affect the endocrine system via estrogenic, androgenic,
antiandrogenic, and antithyroid mechanisms. One key report was a 12
September 1992 review in the British Medical Journal indicating
significant declines in sperm counts in many countries between 1938
and 1990. The findings were controversial because the reviewed studies
used inconsistent designs and methods. In November 1997, however, a
review published in EHP by Swan and others confirmed the findings for
males in the United States and indicated an even sharper decline among
European men. Other studies have found declines for specific areas or
no decline at all.

"I think the evidence across studies is mixed," says Russ Hauser, an
associate professor of environmental and occupational epidemiology at
Harvard School of Public Health. "Historical studies were not designed
to explore this question. It wasn't that someone set out forty or
fifty years ago to design a study to look at how semen quality is
going to change over time." There are going to be limitations in the
data because of that, he explains, so it's hard to determine whether
there is a true temporal trend. "However," he adds, "the data suggest
there are definite geographical differences between countries and
regions within countries in semen quality."

According to Niels Skakkebaek of Rigshospitalet in Copenhagen and
colleagues writing in the February 2006 issue of the International
Journal of Andrology, comparisons of sperm quality among populations
of European men have revealed that as many as 30% of young Danish men
have low sperm count, and an additional 10% may be infertile. Denmark
also has an unusually high rate of testicular cancer. Rates have been
increasing in many countries over the last 50 years, but the Danish
rate is noticeably higher; for example, four to five times higher than
the Finnish rate.

This difference prompted researchers to also examine incidence of
hypospadias (in which the urethra opens along the underside of the
penis shaft rather than the tip) and cryptorchidism. Not only did both
disorders occur more frequently in Danish boys compared with Finnish
boys, but the Danish rates had risen in recent decades. These findings
as a whole inspired Skakkebaek and colleagues to propose, in the May
2001 issue of Human Reproduction, an overarching disorder, testicular
dysgenesis syndrome (TDS), in which perturbation of testis development
in fetal life sets the stage for hypospadias, cryptorchidism,
testicular cancer, and reduced sperm quality.

It's reasonable to suspect there might be a female corollary to TDS.
"We have no really good reasons not to expect that women are as
sensitive to environmental chemicals as the males are," says Jens
Peter Bonde, a professor of occupational medicine at Arhus University
Hospital in Copenhagen. He points out that it's easier to study male
fertility because men can easily provide sperm samples. "That's one
basic reason that there has been so much attention on the males, but
from a biological point of view one would definitely expect that the
female reproductive system might be vulnerable also," says Bonde.

According to Guillette, another stumbling block is the accepted, but
unproven, dogma that an embryo will develop as a normal female barring
any hormonal signals to become male. "It hasn't been an area where
there have been substantial amounts of work done. There's certainly
very good work, but not the same kind of huge body of literature that
one sees about the developing testis and the male reproductive
system," he says.

His side. Male infertility can arise from factors such as low sperm
count and sperm abnormalities including altered morphology and low
motility. Up to 10% of infertility cannot be explained medically.
image: Christian Darkin/Shutterstock

One of the few epidemiologic studies to link low-level human exposure
to an environmental contaminant with a specific end point was Swan and
colleagues' investigation of prenatal phthalate exposure, published in
the August 2005 issue of EHP. Their results suggested a subtle change
in boys' development -- a shortening of the anogenital index (the
distance between the anus and the scrotum, divided by weight) --
associated with prenatal exposure to several phthalates. This finding
is not a predictor of future fertility and needs confirmation, but it
is noteworthy as the first study to link verified prenatal exposure to
a specific outcome.

Animal Findings to Human Concerns?

Consequences of disrupting the normal hormone milieu have also been
observed in wildlife. Examining alligators in polluted lakes in
northern Florida, Guillette's group has observed altered function of
the ovaries and testes, smaller penis size, and abnormalities that
extend to the thyroid gland, liver, and immune system. A robust body
of literature details reproductive effects in fish, amphibians, and
reptiles related to their exposure to endocrine disruptors. Evidence
of these effects has also been seen in wild mammals such as polar
bears and seals. Laboratory animal experiments have confirmed these
wildlife findings, demonstrating that effects are not necessarily from
steroid receptor disruption, however, but may, for example, be
observed in altered synthesis and control of endogenous hormones.

The study of fertility also encompasses pregnancy, especially the
early weeks following fertilization. Early pregnancy loss is normally
quite high in humans, with an estimated 30% of pregnancies ending in
miscarriage in the first six weeks. A frequent cause of miscarriage is
aneuploidy, an incorrect number of chromosomes in the embryo, and
mouse studies have shed some light on potential environmental
contributors to this condition.

During a 1998 investigation of age-related aneuploidy rate increases,
Patricia Hunt, a professor of molecular biosciences and a reproductive
biologist at Washington State University, and her colleagues were
amazed to see a sudden rate spike in their mouse colony. An
investigation revealed correlation between damage to the plastic mouse
cages and the chromosomal abnormality. Further scrutiny implicated
bisphenol A (BPA), a suspected environmental estrogen used in plastics
manufacture, as the potential causal agent. In a study published in
the 1 April 2003 issue of Current Biology, the researchers replicated
exposure experimentally and found that BPA derailed proper chromosome
segregation during oocyte meiosis.

An extension of this research has been completed with amazing -- but
not yet published -- results, and Hunt hopes that the line of inquiry
can be extended to humans. "One of the things that my new research on
BPA has made me wonder is whether or not there could be environmental
effects that would change the frequency or in specific populations
might cause noticeable differences in aneuploidy," she says.

Hunt says it's hard to know precise numbers of human aneuploidy cases.
"We can't see the loss that occurs preimplantation, but we make an
assumption that there's quite a bit, based on what we can see and what
we think must happen," she says. But whether there's been an increase
in aneuploidy over time cannot be known. "Human aneuploidy studies
were done mostly in the 1970s and early 1980s," says Hunt. "Is this
aneuploidy rate the same across all populations? To the best of our
knowledge, it has been, at least in those previous studies. But is the
rate the same as it was then? We wouldn't know. We wouldn't be able to
see a dramatic increase in chromosomally abnormal spontaneous
abortions, because those kinds of studies aren't currently under way."

The wild side. Animal and wildlife studies of reproductive health
effects, including mouse aneuploidy data, may help inform knowledge of
human effects. Although the reproductive system is highly conserved
across species, differences in exposure, metabolism, and anatomy make
direct interspecies comparisons impossible. image: Getty Images

Extending animal studies to human health is a challenge, though.
Genetically, the reproductive system is highly conserved across
species, making it likely that responses to inputs would be similar.
But species differences in exposure, metabolism, and anatomy preclude
making a direct comparison.

"Wildlife studies cannot be related to humans one to one," says
Guillette. "If one's looking at the functioning of the ovary, or the
functioning of the brain, and hormones, and even the genes that seem
to be involved with the proliferation or the growth of the uterus or
the development of an egg, for example, they're incredibly conserved."
He explains that if problems are seen in these animals at a certain
level, and researchers are able to identify mechanisms that are being
disturbed leading to those abnormalities, then that raises possible
concerns for humans, even if humans are exposed in a slightly
different manner.

Worldwide Concerns

Geographic differences may suggest environmental exposures that need
investigation, wrote Swan in a paper published in the February 2006
issue of Seminars in Reproductive Medicine. For example, in the first
phase of the EPA-funded Study for Future Families, of' which Swan is
the principal investigator, she and her colleagues saw significant
reductions in sperm concentration, motility, and total motile sperm in
men from Columbia, Missouri, compared with men in New York City,
Minneapolis, and Los Angeles. In an in-depth follow-up study comparing
variables between the Columbia and Minneapolis men, the researcher
discovered that the Missouri group had had higher exposure to
agricultural pesticides. Further, men with low sperm counts were more
likely to have higher urine metabolite levels of the pesticides
alachlor, atrazine, metolachlor, and diazinon.

Another geographically based study, INUENDO, investigates risks to
human fertility from persistent environmental organochlorines. The
European Commission project centers on Arctic populations including
Swedish fishermen and the Inuit of North America and Greenland, whose
exposure to persistent organic pollutants such as PCBs and DDT
metabolites are among the highest in the world. "There are many
indications from animal studies and from wildlife studies, but very
few indications from human studies telling us whether we have a
problem or not," says Bonde, who serves as coordinator of INUENDO.

"The basic idea [behind INUENDO] was to go to places in the world
where we know that people have high level of exposures to substances
that are suspected to cause these effects in fertility," says Bonde.
"That's the reason we went to Greenland and to Sweden, where fishermen
are known to have very high exposure levels; we have other populations
that have lower levels of exposures, so we have contrasts of
exposure." Results published in March 2006 in Human Reproduction
suggested a longer time to pregnancy related to serum concentrations
of PCB and DDE in mothers and fathers. Additional results published in
the May 2006 EHP suggested an altered sex ratio of offspring (fewer
boys than would otherwise be expected) related to PCB and DDE

Exploring multicompound exposures is yet another challenge in
environmental epidemiology. "Individuals are exposed to many different
phthalates, a variety of persistent and nonpersistent pesticides,
different patterns of PCB congeners, as well as other chemicals," says
Hauser. "How do we take all that information, based on the chemical
assessment in urine or in blood, and use that to assign exposure for
that individual to ten, or twelve, or many more different compounds?"
he says. In the April 2005 issue of EHP, Hauser's group described
evidence suggesting a relationship between PCBs and phthalates and
human sperm motility, possibly due to PCBs' inhibiting a key enzyme in
phthalate metabolism.

Genes themselves offer another platform for investigation. Hugh
Taylor, director of the Yale Center for Research in Reproductive
Biology, leads a team investigating the role of estrogen-regulated Hox
genes that direct uterine development. The researchers initially
focused on DES effects and discovered that the compound alters
expression of the Hoxa10 gene in mice, affecting the tissue type that
grows in the uterus, cervix, and vagina. Effects were triggered only
with exposure during development, but not during adulthood, and later
experiments revealed that the pesticide methoxychlor had similar

"The important thing is that these agents really seem to imprint the
expression pattern, even long after the agent is removed or there's no
longer an exposure," says Taylor. "When we have a clear-cut animal
model and know the genes that are affected, we can start to think
about evaluating that exposure by looking for changes in the gene
expression earlier and see if it has a significant effect rather than
waiting a whole generation."

A view inside. Understanding that a person's reproductive health can
be linked to the very earliest of exposures, possibly even paternal or
maternal exposures prior to conception, points up the critical need to
elucidate the health effects of environmental chemicals. image:

This is a goal of research in epigenetics, the study of how genetic
messages may be edited through methylation or other means without
changing the actual DNA sequence. For example, Rebecca Sokol and
colleagues at the University of Southern California are currently
investigating whether DNA methylation in sperm might serve as a
biomarker of environmental exposure and a means of assessing male
fertility. Additionally, preliminary work at Washington State
University and at the NIEHS indicates that an epigenetic event in one
generation can "reprogram" the germline and affect later generations.
In essence, the exposures of one's great-grandparents could still
matter today.

Expanding Understanding

Previous generations' exposures would be useful information to have,
according to Hunt. "What we really need is data on generations ago,
and we simply don't have that data," she says. "We have to wait a
generation to see. We have to wait until... young exposed males grow
up to the point where we can assess sperm counts."

This will require prospective studies to determine early exposures.
"If you want to look at fertility -- and it's difficult to do -- you
ideally would want to do a study in which you start assessing
environmental exposures preconception," says Hauser. "You'd have to
identify couples who are thinking of trying to conceive and try to
understand their environmental exposures, and then follow them forward
in time."

According to Alison Carlson, a senior fellow at The Collaborative on
Health and the Environment (CHE) in Bolinas, California, another need
is very basic: tracking the incidences of infertility and common known
causes. "For us to try to make headway studying environmental
influences on fertility, it's really hard when we don't have good
baseline data," she says. "We don't know the real incidence and
prevalence rates of premature ovarian failure and polycystic ovarian
syndrome and lots of other end points that people study. We don't know
what they are, so how can we study trends and the environmental
contributions?" she asks.

A thorough exploration of environmental effects on fertility will
require the expertise of demographers, epidemiologists, clinicians,
biologists, wildlife researchers, geneticists, molecular biologists,
exposure assessment specialists, toxicologists, and others -- and
discussion requires someone "to set the table," says Carlson. A
February 2005 workshop titled "Understanding Environmental
Contaminants and Human Fertility Compromise: Science and Strategy"
demonstrated multidisciplinary fervor for investigation, and a more
in-depth conference, the "Summit on Environmental Challenges to
Reproductive Health and Fertility," cosponsored by CHE and the
University of California, San Francisco, is scheduled for 28-30
January 2007. "Reproduction is such a human, deep-seated, deeply
psychically coded thing," says Carlson. "It's hard not to care about
fertility compromise."

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From: Tolerance.org, Mar. 6, 2003
[Printer-friendly version]


By Tim Wise

Ask a fish what water is and you'll get no answer.

Even if fish were capable of speech, they would likely have no
explanation for the element they swim in every minute of every day of
their lives. Water simply is. Fish take it for granted.

So too with this thing we hear so much about, "racial preference."
While many whites seem to think the notion originated with affirmative
action programs, intended to expand opportunities for historically
marginalized people of color, racial preference actually has had a
long and very white history.

Affirmative action for whites was embodied in the abolition of
European indentured servitude, which left black (and occasionally
indigenous) slaves as the only unfree labor in the colonies that would
become the U.S.

Affirmative action for whites was the essence of the 1790
Naturalization Act, which allowed virtually any European immigrant to
become a full citizen, even while blacks, Asians and American Indians
could not.

Affirmative action for whites was the guiding principle of
segregation, Asian exclusion laws, and the theft of half of Mexico for
the fulfillment of Manifest Destiny.

In recent history, affirmative action for whites motivated racially
restrictive housing policies that helped 15 million white families
procure homes with FHA loans from the 1930s to the '60s, while people
of color were mostly excluded from the same programs.

In other words, it is hardly an exaggeration to say that white America
is the biggest collective recipient of racial preference in the
history of the cosmos. It has skewed our laws, shaped our public
policy and helped create the glaring inequalities with which we still

Income and inheritance

White families, on average, have a net worth that is 11 times the net
worth of black families, according to a recent study; and this gap
remains substantial even when only comparing families of like size,
composition, education and income status.

A full-time black male worker in 2003 makes less in real dollar terms
than similar white men were earning in 1967. Such realities are not
merely indicative of the disadvantages faced by blacks, but indeed are
evidence of the preferences afforded whites -- a demarcation of
privilege that is the necessary flipside of discrimination.

Indeed, the value of preferences to whites over the years is so
enormous that the current baby-boomer generation of whites is
currently in the process of inheriting between $7 trillion and $10
trillion in assets from their parents and grandparents -- property
handed down by those who were able to accumulate assets at a time when
people of color by and large could not.

To place this in the proper perspective, we should note that this
amount of money is more than all the outstanding mortgage debt, all
the credit card debt, all the savings account assets, all the money in
IRAs and 401k retirement plans, all the annual profits for U.S.
manufacturers, and our entire merchandise trade deficit combined.

Yet few whites have ever thought of our position as resulting from
racial preferences. Indeed, we pride ourselves on our hard work and
ambition, as if somehow we invented the concepts.

As if we have worked harder than the folks who were forced to pick
cotton and build levies for free; harder than the Latino immigrants
who spend 10 hours a day in fields picking strawberries or tomatoes;
harder than the (mostly) women of color who clean hotel rooms or
change bedpans in hospitals, or the (mostly) men of color who collect
our garbage.

We strike the pose of self-sufficiency while ignoring the advantages
we have been afforded in every realm of activity: housing, education,
employment, criminal justice, politics, banking and business.

We ignore the fact that at almost every turn, our hard work has been
met with access to an opportunity structure denied to millions of
others. Privilege, to us, is like water to the fish: invisible
precisely because we cannot imagine life without it.

The point of points

It is that context that best explains the duplicity of President
Bush's recent criticisms of affirmative action at the University of

President Bush, himself a lifelong recipient of affirmative action --
the kind set aside for the mediocre rich -- recently proclaimed that
the school's policies were examples of unfair racial preference.

Yet in doing so he not only showed a profound ignorance of the
Michigan policy but also made clear the inability of yet another white
person to grasp the magnitude of white privilege still in operation.

The President attacked Michigan's policy of awarding 20 points (on a
150-point evaluation scale) to undergraduate applicants who are
members of underrepresented minorities (which at U of M means blacks,
Latinos and American Indians). To many whites such a "preference" is
blatantly discriminatory.

Bush failed to mention that greater numbers of points are awarded for
other things that amount to preferences for whites to the exclusion of
people of color.

For example, Michigan awards 20 points to any student from a low-
income background, regardless of race. Since these points cannot be
combined with those for minority status (in other words poor blacks
don't get 40 points), in effect this is a preference for poor whites.

Then Michigan awards 16 points to students who hail from the Upper
Peninsula of the state: a rural, largely isolated and almost
completely white area.

Of course both preferences are fair, based as they are on the
recognition that economic status and even geography (as with race) can
have a profound effect on the quality of K-12 schooling that one
receives, and that no one should be punished for things that are
beyond their control.

But note that such preferences -- though disproportionately awarded to
whites -- remain uncriticized, while preferences for people of color
become the target for reactionary anger. Once again, white preference
remains hidden because it is more subtle, more ingrained and isn't
called white preference, even if that's the effect.

But that's not all. Ten points are awarded to students who attended
top-notch high schools, and another eight points are given to students
who took an especially demanding AP and honors curriculum.

As with points for those from the Upper Peninsula, these preferences
may be race-neutral in theory, but in practice they are anything but.

Because of intense racial isolation (and Michigan's schools are the
most segregated in America for blacks, according to research by the
Harvard Civil Rights Project), students of color will rarely attend
the "best" schools, and on average, schools serving mostly black and
Latino students offer only a third as many AP and honors courses as
schools serving mostly whites.

So even truly talented students of color will be unable to access
those extra points simply because of where they live, their economic
status and ultimately their race, which is intertwined with both.

Four more points are awarded to students who have a parent who
attended the U of M: a kind of affirmative action with which the
President is intimately familiar, and which almost exclusively goes to

Ironically, while alumni preference could work toward the interest of
diversity if combined with aggressive race-based affirmative action
(by creating a larger number of black and brown alums), the rollback
of the latter, combined with the almost guaranteed retention of the
former, will only further perpetuate white preference.

So the U of M offers 20 "extra" points to the typical black, Latino or
indigenous applicant, while offering various combinations worth up to
58 extra points for students who will almost all be white. But while
the first of these are seen as examples of racial preferences, the
second are not, hidden as they are behind the structure of social
inequities that limit where people live, where they go to school, and
the kinds of opportunities they have been afforded.

Undercurrents of privilege

White preferences, the result of the normal workings of a racist
society, can remain out of sight and out of mind, while the power of
the state is turned against the paltry preferences meant to offset

Very telling is the oft-heard comment by whites, "If I had only been
black I would have gotten into my first-choice college."

Such a statement not only ignores the fact that whites are more likely
than members of any other group -- even with affirmative action in
place -- to get into their first-choice school, but it also presumes,
as anti-racist activist Paul Marcus explains, "that if these whites
were black, everything else about their life would have remained the

In other words, that it would have made no negative difference as to
where they went to school, what their family income was, or anything

The ability to believe that being black would have made no difference
(other than a beneficial one when it came time for college), and that
being white has made no positive difference, is rooted in privilege
itself. The privilege that allows one to not have:

** to think about race on a daily basis;

** one's intelligence questioned by best-selling books;

** to worry about being viewed as a "out of place" when driving,
shopping, buying a home, or for that matter, attending the University
of Michigan.

So long as those privileges remain firmly in place and the
preferential treatment that flows from those privileges continues to
work to the benefit of whites, all talk of ending affirmative action
is not only premature but a slap in the face to those who have fought,
and died, for equal opportunity.

Tim Wise is an antiracist activist, essayist and lecturer. This
article was reprinted with permission from Alternet.

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