Liberty Goodwin, Director

P.O. Box 40441, Providence, RI 02940

Tel. 401-351-9193, E-Mail:


(Lighting the Way to Less Toxic Living)




EXCERPTED FROM:  Neurodevelopment And Endocrine Disruption, Theo Colborn, Department of Zoology, University of Florida, Gainesville, Florida, and The Endocrine Disruption Exchange, Paonia, Colorado

Environmental Health Perspectives: Annual Review Issue Volume 112, Number 9, June 2004,   Address correspondence to T. Colborn, P.O. Box 1253, Paonia, CO 81428.  Telephone/Fax: (970) 527-6548. E-mail:


IMPORTANT NOTE:  This is greatly reduced from a long and well-researched article.  We urge you to access the original, at the link above, for much more information and scholarly references.


Abstract:  In this article I explore the possibility that contaminants contribute to the increasing prevalence of attention deficit hyperactivity disorder, autism, and associated neuro-developmental and behavioral problems in developed countries.  I discuss the exquisite sensitivity of the embryo and fetus to thyroid disturbance and provide evidence of human in utero exposure to contaminants that can interfere with the thyroid.  Because it may never be possible to link prenatal exposure to a specific chemical with neurodevelopmental damage in humans, I also present alternate models where associations have been made between exposure to specific chemicals or chemical classes and developmental difficulties in laboratory animals, wildlife, and humans. 


Introduction:  Approximately 12 years ago the scientific community acknowledged that certain synthetic chemicals are capable of crossing the placental and brain barriers and interfering with development and function (Colborn and Clement 1992).  The chemicals mimic or interfere with endogenous hormones and other signaling chemicals of the endocrine system. These chemicals, distinguished as endocrine disruptors, bridge many chemical classes and are an integral part of the world economy and commerce. To date no validated or standardized screens or assays have been developed to test chemicals for their possible endocrine-disrupting effects.  Consequently, none of the thousands of chemicals used today have been tested systematically for these effects for regulatory purposes.  Despite this, the list is growing of known endocrine disruptors having a wide range of mechanisms of action that can interfere with brain development.


Historical Perspective of Exposure and Human Disorders:  When data on the growth in synthetic chemical production are compared with the data on increasing prevalence of neuro-developmental and other developmental disorders in humans, the data begin to merge around 1970.  At approximately the same time, the first generation of humans exposed in the womb to synthetic chemicals on a large scale began to have children of their own.  For example, a plastic monomer, bisphenol A (BPA), was introduced in the early 1920s. Polychlorinated biphenyls (PCBs) were introduced in 1929.  DDT became available for retail sale in 1938, and the large-scale, widespread commercial use of a vast number of synthetic chemicals commenced near the end of World War II (WWII) in the 1940s.  Although individuals were being exposed to these chemicals since the early 1920s, it was not until the end of WWII that exposure increased to such an extent that vast numbers of adults exposed daily were accumulating significant amounts of these chemicals in their bodies. In terms of generation time, these individuals in the 1950s produced the first generation of offspring exposed to numerous synthetic chemicals in the womb and at increased levels.  By 1970 these post-WWII babies were having children of their own. It was during the 1970s that what appeared to be increases in unusual, previously rare neuro-developmental disorders began to catch the attention of health professionals.


Sensitivity of Neurodevelopment to Thyroid Hormones:  Although it has been known for a century that hypothyroidism leads to retardation and other serious developmental effects, the role of thyroid hormones in brain development is still not completely understood.  It is also accepted that thyroid hormones transferred from the mother to the embryo and fetus are critical for normal brain development, even though the thyroid gland of a fetus starts producing thyroid hormones at about 10 weeks.  We now recognize that only a slight difference in the concentration of thyroid hormones during pregnancy can lead to significant changes in intelligence in children. 


Overcoming the Difficulty of Making Causal Links:  It is almost impossible to make causal links between prenatal contaminant exposure and developmental damage in humans. Because of this, scientists have used laboratory and wild-animal models to better understand the effects of synthetic chemicals on development.  For example, reports of serious developmental and reproductive problems among birds in the North American Great Lakes and other regions in developed countries date back to the 1960s and early 1970s.  Thyroid gland and hormone abnormalities in particular were repeatedly reported in Great Lakes herring gulls used in a Canadian monitoring program to track PCBs and other organochlorine chemicals in the lakes.


The Human Connection:  In the Lake Michigan study trained psychologists were able to measure developmental delays in infants shortly after birth if the blood fat of the mother held 1.00 parts per million (ppm) PCBs (Jacobson and Jacobson 1996). At 1.25 ppm PCBs, the change was statistically significant (p < 0.001) because there was so little variance. The intelligence and behavioral impairments reported in this study are population-wide.  They are not rare events such as cancer. In this healthy mother-infant study, at 11 years of age, 11% of the children were affected (Jacobson and Jacobson 1996).  At 4 years of age, 17 children were removed from the study because they were too hyperactive and would not take the tests (Jacobson et al. 1990). If the outliers had remained in the study, 20% of the children would have been affected. It was later determined that the children who were removed from the study were the children of the mothers with the highest PCB concentrations in the study. Another child was removed from the study at the end because he or she had an IQ below 70 (Jacobson and Jacobson 1996). These researchers noted that consuming fish is not the only source of PCBs, but these compounds are found in many other foods such as meats, fatty foods, fast foods, cheeses, ice cream, and even in the most rigid vegan diet (Schecter et al. 2001).


Opening the Black Box of Exposure:  Fortunately, in the past 5 years, technology for measuring human exposure to synthetic chemicals has advanced considerably.  For example, the CDC can now monitor human blood and urine for > 116 chlorinated and nonchlorinated chemicals and their metabolites.  These include contemporary-use pesticides and industrial chemicals used in cosmetics, perfumes, detergents, toys, plastics, and fire retardants--many of which are high-production-volume chemicals widely used in commerce.  CDC chemists have begun to open the black box of exposure not only for a better picture of human organochlorine chemical exposure but for a number of other widely used chemicals that have not been studied as intensely. For example, they discovered that some metabolites of a class of chemicals called phthalates were 9 times higher in the urine of women between 20 and 40 years of age--women of childbearing age--than in any other segment of the population (Blount et al. 2000).  Phthalates make plastics flexible and soft; they are used to improve delivery systems in perfumes, nail polish, shampoos, cosmetics, and dermal and intravenous applications of medications.  They have been widely used as inert ingredients in pesticide formulations.  Three of the phthalates, diethylhexyl phthalate, di(n-octyl) phthalate, and di(n-hexyl) phthalate, are antiandrogens in laboratory animals, producing hypospadias, cryptorchidism, and other male developmental disorders.  They also interfere with the thyroid system.


Discussion:  Fortunately, technological improvements in the past 10 years have broadened the scope and sensitivity of detection for not only synthetic chemicals in human tissues but also for natural endogenous hormones.  The evidence that certain hormones operate at parts per trillion and parts per billion and equivalent exposure to endocrine-active chemicals is equivalent or higher reveals the extreme vulnerability of development to chemical perturbation.  During the organizational stages of gestation, responses to endocrine disruption are unlike the typical responses in adulthood.  Consequently, testing with mature animals misses the organizational damage from prenatal exposure.  In addition, most traditional toxicological tests use doses 1,000-1,000,000 times that of the equivalent physiological range at which the endocrine systems operate and well above real-world exposure concentrations to synthetic chemicals.  The high doses used in toxicological testing far exceed the normal threshold or peak concentrations at which homeostatic negative-feedback control from the brain shuts down cellular responses.  Thus, in endocrine disruption, extrapolating down from several high doses to determine the lowest safe dose or no-effect dose of a chemical will not protect the fetus.


FOR INFORMATION ABOUT ENDOCRINE-DISRUPTING CHEMICALS IN CHILDREN’S PRODUCTS, AS WELL AS LEGISLATIVE AND OTHER ACTIONS YOU CAN TAKE, CONTACT: Liberty Goodwin, Director, Toxics Information Project (TIP), Providence, RI, Tel. 401-351-9193, E-Mail,  On the web, visit: &