GMW: A New Way to Inherit Environmental Harm

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GMW: A New Way to Inherit Environmental Harm

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Fri, 22 Jul 2005 19:17:47 +0100

 

 

 

 

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A New Way to Inherit Environmental Harm

Rachel's Environment & Health News, June 9 2005

by Tim Montague

http://www.rachel.org/bulletin/index.cfm?St=3

 

New research shows that the environment is more important to health

than anyone had imagined. Recent information indicates that toxic effects

on health can be inherited by children and grandchildren, even when

there are no genetic mutations involved.[1] These inherited changes are

caused by subtle chemical influences, and this new field of scientific

inquiry is called " epigenetics. " [2]

 

Since the 1940s, scientists have known that genes carry information

from one generation to the next, and that genes gone haywire can cause

cancer, diabetes, and other diseases. But scientists have also known that

genes aren't the whole story because identical twins -- whose genes are

identical --can have very different medical histories. One identical

twin can be perfectly healthy while the other develops schizophrenia or

cancer -- so the environment must play a significant role, not merely

genes.

 

What's surprising is that scientists are now revealing that these

environmental effects can be passed from one generation to the next by a

process called " epigenetics, " with far-reaching implications for human

health. Epigenetics is showing that environmental influences can be

inherited -- even without any mutations in the genes themselves[1] --

and may

continue to influence the onset of diseases like diabetes, obesity,

mental illness and heart disease, from generation to generation.

 

In other words, the cancer you get today may have been caused by your

grandmother's exposure to an industrial poison 50 years ago, even though

your grandmother's genes were not changed by the exposure.[1] Or the

mercury you're eating today in fish may not harm you directly, but may

harm your grandchildren.

 

This emerging field of epigenetics is causing a revolution in the

understanding of environmental influences on health. The field is only

about

20 years old, but is becoming well-established. In 2004, the National

Institutes of Health granted $5 million to the Johns Hopkins Medical

School in Baltimore to start the Center for Epigenetics of Common Human

Disease.

 

The latest information appears in a new study by Michael Skinner and

colleagues at Washington State University, published in the June 3 issue

of Science magazine. Skinner found that mother rats exposed to

hormone-mimicking chemicals during pregnancy gave birth to four

successive

generations of male offspring with significantly reduced fertility.[3]

Only

the first generation of mothers was exposed to a toxin, yet four

generations later the toxic effect could still be detected.

 

Prior to this study, scientists had only been able to document

epigenetic effects on the first generation of offspring. These new

findings

suggest that harm from toxins in the environment can be much longer

lasting and pervasive than previously known because they can impact

several

generations.

 

And therefore a precautionary approach to toxics is even more important

that previously believed. (See Rachel's 765, 770, 775, 781, 787, 789,

790, 791, 802, 803, 804.)

 

Over the past sixty years doctors and scientists have pieced together a

picture of the genetic basis for life and some of the genetic causes

of! human and animal disease. Genes regulate the production of proteins

-- the essential building blocks of life. Genes are composed of a finite

series of letters (a code made up of Cs, Ts, As, and Gs, each

representing a nucleotide) embedded in long strands of DNA. DNA is the

large

molecule, composed of genes, that carries the genetic inheritance forward

into the next generation.

 

There are approximately three billion 'letters' in the human genetic

code. Science has long understood that when a gene mutates -- that is,

when a typo is introduced -- it can have far-reaching effects for the

cell, the tissue and the organism as a whole. For example, a genetic

mutation caused by too much sun (ultraviolet radiation), could result in

abnormal uncontrolled cell growth which could lead to skin cancer which

could spread throughout your body. Stay in the shade and you reduce your

risk.

 

But now scientists are seeing that disease can be passed from

generation to generation without any genetic mutations.[1] The DNA

molecule

itself gets another molecule attached to it, which changes the

behavior of

the genes without changing the genes themselves.[1] The attachment of

these additional molecules is caused by environmental influences -- but

these influences can then be passed from one generation to the next, if

they affect the germ cells, i.e., the sperm or the egg.

 

Scientists have, so far, discovered three different kinds of

" epigenetic " changes that can affect the DNA molecule and thus cause

inheritable

changes. One is the methyl molecule.

 

Scientists began to see direct connections between human diseases like

cancer and these subtle genetic variations like methylation in 1983

when Andrew Feinberg and his colleagues at Johns Hopkins found that

cancer

cells had unusually low incidence of DNA-methylation.[4]

 

Methyl is a molecule of one carbon atom and three hydrogen atoms.

Together they attach to a strand of DNA altering its three-dimensional

structure and the behavior of specific genes in the DNA strand. It

turns out

that methylation works like a volume control for the activity of

individual genes. Whereas genetic mutations are typos and relatively

easy to

test for, epigenetic changes are analogous to the formatting of the

text (e.g. font, size, and color) and are much less-well understood. Over

the past 20 years, Feinberg and many other cancer specialists have

documented the wide-spread influence of epigenetics on the development of

cancer in humans and laboratory animals.[5]

 

So epigenetics is changing our traditional picture of common chemicals,

like DDT. DDT is a powerful environmental toxin --once it enters a

living thing it mimics the behavior of natural hormones -- resulting in

abnormal sexual and reproductive development. Widespread use of DDT in

the

1940s and 1950s is associated with large scale declines in some bird

populations (like the Peregrine falcon) because DDT causes birds'

eggshells to thin, and thus the eggs crack before the embryo can

develop into

a chick.

 

When persistent environmental pollutants (like DDT) are phased out, we

might be falsely lulled into believing that we have solved the problem.

The thinking is logical -- remove the toxin from the environment and

you get rid of the toxic effects. Not so according to the findings of

Skinner and his colleagues.

 

The Skinner study tells us that phasing out dangerous toxins doesn't

end the problem -- because the damage done by exposures decades ago could

still flow from generation to generation via epigenetic pathways.

 

Skinner and his colleagues treated groups of pregnant rats, some with

methoxychlor and some with vinclozolin. Methoxychlor is a replacement

for DDT, a pesticide used on crops and livestock and in anima! l feed.

Vinclozolin is a fungicide widely used in the wine industry. It is just

one of a suite of widely used chemicals from flame-retardants to

ingredients in plastics that can cause reproductive abnormalities in

laboratory animals.

 

Both methoxychlor and vinclozolin are known hormone disruptors (see

Rachel's 486, 487, 499, 501, and 547). Male offspring of these

pesticide-treated mothers had reduced fertility (lower sperm count,

reduced sperm

quality), which was not a surprising finding. The scientists then bred

these offspring, and again the male offspring had reduced fertility.

This came as a complete surprise. Over 90% of the male offspring in four

generations of the test animals had reduced fertility.

 

Skinner's report concludes that genetic mutations are highly unlikely

to produce such a strong signal in the treated animals and that

DNA-methylation is the likely mechanism responsible for the observed

decline in

male fertility.

 

Treating the mother rats during pregnancy apparently re-programmed the

genetic material in the male offspring so that all subsequent male

offspring suffered lower fertility from this environmental factor.

 

Skinner believes that his findings in rats could explain the dramatic

rise in breast and prostate cancers in humans in recent decades (see

Rachel's 346, 369, 375, 385 and 547) as partly due to the cumulative

effects of multiple toxins over several generations.

 

Skinner acknowledges that the doses he gave his rats were high,

compared to the doses humans might expect to receive from environmental

exposures. He is continuing his rat experiments with lower doses now.

 

Of course all this new information makes the control of toxic chemicals

even more important that previously thought. The health of future

generations is at stake.

 

The development of epigenetics also greatly complicates toxicity

testing, and chemical risk assessment. Epigenetics tells us that much

additional toxicity testing will be needed. So far, there are no

standardized,

government-approved protocols for conducting epigenetic tests. Until

such protocols emerge (which could take years), and a great deal of

expensive testing has been completed (requiring many more years), risk

assessors will have to acknowledge that -- so far as epigenetics is

concerned -- they are flying blind.

 

* Tim Montague is Associate Director of Environmental Research

Foundation. He holds an M.S. degree in ecology from University of

Wisconsin-Madison and lives in Chicago.

 

[1] Here we define a genetic mutation as a change in the sequence of

nucleotide bases (C,A,T,G). We recognize that epigenetic changes are

heritable changes to the DNA, but they are not sequence changes.

 

[2] To see nine articles on epigenetics from the popular press,

including an excellent series from the Wall Street Journal, go to

http://www.rachel.org/library/getfile.cfm?ID=531

 

[3] M. Anway, A. Cupp, M. Uzumcu, and M. Skinner, " Epigenetic

Transgenerational Actions of Endocrine Disruptors and Male Fertility, "

SCIENCE

Vol. 308 (June 3, 2005), pgs. 1466-1469. Michael Skinner is director of

Washington State University's Center for Reproductive Biology;

http://www.skinner.wsu.edu

 

[4] Andrew Feinberg and Bert Vogelstein, " Hypomethylation distinguishes

genes of some human cancers from their normal counterparts, " NATURE

Vol. 301 (January 6, 1983), pgs. 89-92.

 

[5] Andrew Feinberg and Benjamin Tycko, " The history of cancer

epigenetics, " NATURE REVIEWS (February 2004) Vol. 4, pgs. 143-153.

 

 

 

 

 

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