INFOTERRA: Fw: Rachel #757: From Silent Spring to Scientific Revolution, Pt. 1
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Subject: Rachel #757: From Silent Spring to Scientific Revolution, Pt. 1
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> =======================Electronic Edition====================
> . .
> . RACHEL'S ENVIRONMENT & HEALTH NEWS #757 .
> . ---November 28, 2002--- .
> . HEADLINES: .
> . FROM SILENT SPRING TO SCIENTIFIC REVOLUTION .
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>
> FROM SILENT SPRING TO SCIENTIFIC REVOLUTION -- PART 1
>
> [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
> humans.[2,3] 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
> PERSPECTIVES, HUMAN REPRODUCTION, TOXICOLOGY,
> and ENVIRONMENTAL SCIENCE AND TECHNOLOGY.
>
> 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
> behaviors.
>
> 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
> variables.
>
> 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
> detail.
>
> ===========================================
>
> 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
> exposure.
>
> 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
> chemicals.
>
> 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
> process.
>
> ===========================================
>
> 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
> http://www.ProtectingOurHealth.org.
>
> [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.
> ENVIRONMENTAL HEALTH PERSPECTIVES 110: pgs. A593-A598.
>
> [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
> Dutch Preschool Children. ENVIRONMENTAL HEALTH PERSPECTIVES
> 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
> relevant doses. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES
> (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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