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#757 - From Silent Spring to Scientific Revolution -- Part 1, 27-Nov-2002

[This essay first appeared in SAN FRANCISCO MEDICINE, November
2002. See http://www.sfms.org/sfm/ for other important work. In
the text, I have added explanatory notes inside square brackets,
and the sub-headings have been added as well. For additional
documents and discussions related to these topics, see
http://www.OurStolenFuture.org and
http://www.ProtectingOurHealth.org . --Peter Montague, editor]

by John Peterson Myers*

Four decades ago in SILENT SPRING, Rachel Carson wove together a
fabric of evidence suggesting that parts of the modern chemical
revolution were having unintended consequences, undermining human
and wildlife health in unexpected ways.[1] At the time that
fabric was more Chantilly lace than Afghan rug, with the
scientific pattern defined as much by the holes as by the threads
of connecting evidence.

Her thesis was compelling, nonetheless. It launched the modern
environmental movement. It stimulated a new branch of government
focused on environmental impacts. It led to bans of DDT and,
since then, a host of other chemicals. Most recently it spurred
in 2001 a global treaty, the Stockholm Convention, that requires
phase-out and elimination of twelve persistent organic
pollutants. And it forced new scientific questions to be asked
about links between contamination and health.

We're in the Midst of a Scientific Revolution

Now four decades later, we are midstream in the scientific
revolution that her work helped foment. The revolution arises
from scientific discoveries which establish that many chemicals
-- both from the natural world and synthesized in laboratories --
interfere with the biochemical messaging systems that direct the
biological development of plants and animals, including

Chemicals Can Disrupt Biological Signals

Virtually all biological development is under the control of
various biochemical messaging systems that are involved in the
chain of events leading to gene activation and expression.
Hormones and growth factors, among others, are key elements of
these message systems. Normal healthy development depends on the
successful initiation of genetic instructions by hormones and
growth factors, among others, which are key elements in these
message systems. Disruption can cause immediate effects, ranging
from conspicuous teratological [birth defect] impacts to subtle
functional disabilities that may not be evident until decades
after exposure.

Research now demonstrates that a wide array of chemicals can
disrupt these messages without damaging the genes themselves.
Much attention has focused on disruption of hormonal signaling,
which has become known as endocrine disruption.[4]

Chemicals Can Impair Growth and Development

Investigation of developmental disruption has burgeoned during
the past decade because of research funding by European, Japanese
and North American governments. New results are published
virtually every week in journals like ENVIRONMENTAL HEALTH

For example, a study published in September 2002 by a research
group in the Netherlands documented associations between
variations in background levels of in utero [in the womb]
exposure to certain organochlorine chemicals and gender-specific
play behavior in children.[5] Boys with relatively higher levels
of PCB exposure were less likely to engage in play behaviors
typical for boys; girls more likely to engage in play behavior
typical for boys. Boys with relatively higher levels of dioxin
were more likely to engage in more feminine play behaviors, as
were girls.

These findings are especially noteworthy because the levels of
exposure were not that high, but instead represented variations
around background levels common in European women. Moreover,
these outcomes are consistent with experiments carried out with
laboratory animals examining exposure impacts on sex-specific

The same research group had recently published studies
demonstrating impacts of in utero [in the womb] exposure on
cognitive development and immune system function.[6,7,8] Their
groundbreaking studies rest on detailed tracking of the
development of a cohort [group] of individuals beginning with
measurements of the mother's serum [blood] contamination during
pregnancy, with careful attention paid to potential confounding

A Revolution in Thinking about Health & Environment

New results like these are legion.[9] They are forcing a series
of conceptual shifts upon toxicology as it integrates these new
findings with long-standing assumptions. These shifts are
summarized in Table 1. The text below examines several in greater


Table 1. Conceptual Shifts in Scientific Thinking

1. OLD: High level contamination overwhelms detoxification and
other defense mechanisms. NEW: Low level contamination hijacks
control of development.

2. OLD: The dose makes the poison. NEW: Non-monotonic dose
response curves are common, in which low level exposures cause
effects that disappear at higher levels. [See text for the
meaning of non-monotonic.]

3. OLD: Only high levels of exposure matter. NEW: Impacts caused
at what had been assumed to be background levels.

4. OLD: Focus on adults. NEW: Periods of rapid growth and
development (prenatal through puberty) are most sensitive to

5. OLD: A small number of bad actors. NEW: Many chemicals thought
safe are biological active and capable of interfering with
signaling systems.

6. OLD: Immediate cause and effect. NEW: Long latencies are
common; fetal programming can lead to disease and disabilities
decades later.

7. OLD: Examine chemicals one compound at a time. NEW: In real
life, mixtures are the rule. They can lead to effects at much
lower levels than indicated by simple experiments with single

8. OLD: Focus on traditional toxicological endpoints like
mutagenesis carcinogenesis, cell death. NEW: Wide range of health
endpoints, including immune system dysfunction (both hyper and
hypo-active); neurological, cognitive and behavioral effects;
reproductive dysfunctions; chronic diseases.

9. OLD: One-to-one mapping of contaminant to disease or
disability. NEW: Same contaminant can cause many different
effects, depending upon when exposure occurs during development
and what signals it disrupts. Multiple contaminants can cause
same endpoint [effect], if they disrupt the same developmental


Newly Discovered Effects of Low-Dose Exposures

Traditional toxicology focuses on damage, such as cell death,
mutations or genotoxicity [harm to genes] that occurs typically
when cellular biochemical defense mechanisms are overwhelmed. At
high exposure levels many chemicals implicated in message
disruption are toxic in these traditional ways. At lower levels
of exposure, however, their impacts instead involve, in essence,
hijacking control of development, adding or subtracting to the
body's own control signals at remarkably low levels of exposure.
A vivid recent example is the discovery that a widely used
herbicide, atrazine, causes tadpoles to develop into
hermaphroditic adults [adults with the sex organs of both males
and females in the same individual] at a level of exposure
approximately 30,000 times lower than traditional toxicological
work had identified as toxic to frogs.[10] The mechanism appears
to involve enhancement of aromatase conversion of testosterone to
estrogen during development. [In other words, the common weed
killer, atrazine, seems to cause more male sex hormone to be
changed into female sex hormone, upsetting the normal balance of
the two hormones, thus creating individual tadpoles with both
male and female sex organs.] Elegant theoretical and empirical
work suggests that for activated signaling systems, there may be
no threshold beneath which no effect occurs.[11] [In other words,
if a chemical interferes with the body's hormone signaling
systems, any amount might cause some interference; the only
"safe" dose of such a chemical would be zero.]

[To be continued in RACHEL'S #758.]


* John Peterson Myers, Ph.D., is co-author of OUR STOLEN FUTURE
(paperback: Plume, 1997; ISBN 0452274141), Senior Advisor to the
United Nations Foundation and Senior Fellow, Commonweal, Bolinas,
California. See http://www.OurStolenFuture.org and

[1] Carson, Rachel. 1962. SILENT SPRING. Houghton Mifflin.

[2] Cheek, Ann O., Peter M. Vonier, Eva Oberdorster, Bridgette C.
Burow and John A. McLachlan. 1999. Environmental Signaling: A
Biological Context for Endocrine Disruption. ENVIRONMENTAL HEALTH
PERSPECTIVES 106 Suppl 1. pgs. 5-10.

[3] McLachlan, John A. 2001. Environmental Signaling: What
Embryos and Evolution Teach Us About Endocrine Disrupting
Chemicals. ENDOCRINE REVIEWS 22(3): pgs. 319-341.

[4] Colborn, Theo, Dianne Dumanoski and John Peterson Myers.
1996. OUR STOLEN FUTURE. Dutton.

[5] Vreugdenhil, HJI, FME Slijper, PGH Mulder, and N
Weisglas-Kuperus 2002. Effects of Perinatal Exposure to PCBs and
Dioxins on Play Behavior in Dutch Children at School Age.

[6] Huisman, M, C Koopman-Esseboom, CI Lanting, C G van der
Paauw, L GM Th. Tuinstra, V Fidler, N Weisglas Kuperus, PJJSauer,
ER Boersma and BCL Towen. 1996. Neurological condition in
18-month-old children perinatally exposed to polychlorinated
biphenyls and dioxins. EARLY HUMAN DEVELOPMENT 43: pgs. 165-176.

[7] Koopman-Esseboom, C, N Weisglas-Kuperus, MAJ de Ridder, CG
Van der Paauw, LGM Th Tuinstra, and PJJ Sauer. 1996. Effects of
Polychlorinated Biphenyl/Dioxin Exposure and Feeding Type on
Infants' Mental and Psychomotor Development. PEDIATRICS 97(5):
pgs. 700-706.

[8] Weisglas-Kuperus, N, S Patandin, GAM Berbers, TCJ Sas, PGH
Mulder, PJJ Sauer and H Hooijkaas. 2000. Immunologic Effects of
Background Exposure to Polychlorinated Biphenyls and Dioxins in
108: pgs. 1203-1207.

[9] Myers, J.P. 2002. http://www.OurStolenFuture.org. [This
website is an electronic portal to a wide array of emerging
original research on message disruption.]

[10] Hayes, TB, A Collins, M Lee, M Mendoza, N Noriega, AA
Stuart, and A Vonk. 2002. Hermaphroditic, demasculinized frogs
after exposure to the herbicide, atrazine, at low ecologically
(US) 99: pgs. 5476-5480.

[11] Sheehan, DM, E Willingham, D Gaylor, JM Bergeron and D
Crews. 1999. No threshold dose for estradiol-induced sex reversal
of turtle embryos: how little is too much? ENVIRONMENTAL HEALTH
PERSPECTIVES 107: pgs. 155-159.

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