#757 - From Silent Spring to Scientific Revolution -- Part 1, November 28, 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 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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For additional articles like this one, go to the Tittabawasse River Watch web site www.trwnews.org for complete coverage of the Tittabawassee River Dow Chemical dioxin contamination saga.. The source organization's web site link is listed above. The Newspaper / Media page of our site contains an extensive archive of media articles dating back to January 2002. The Newspaper / Media page may be accessed by scrolling down to the bottom of the CONTENTS section and clicking on the Newspaper/Media link.