Our Stolen Futurea book by Theo Colborn, Dianne Dumanoski, and John Peterson Myers
 
 

 

 

An excerpt from Chapter 10, Altered Destinies

 

 
 


Our fears about toxic chemicals have typically centered around cancer and other physical illnesses. But as one surveys the scientific literature, it becomes quickly apparent that physical disease or visible birth defects may not be the most immediate danger. Long before concentrations of synthetic chemicals reach sufficient levels to cause obvious physical illness or abnormalities, they can impair learning ability and cause dramatic, permanent changes in behavior, such as hyperactivity. Save for a few compounds such as PCBs, we know virtually nothing about the neurological hazards posed by the thousands of synthetic chemicals in commerce.

What little we do know about those few chemicals that have been studied has alarming implications. Both animal experiments and human studies report behavioral disorders and learning disabilities similar to those reported with increasing frequency among school children across the nation. In the United States, an estimated six to ten percent of children under the age of thirteen suffer from a suite of symptoms related to hyperactivity and attention deficit that make it difficult for them to pay attention and learn. Countless others experience learning problems ranging from difficulties with memory to impaired fine motor skills that make it harder to hold a pen and learn how to write.

Scientists still do not have a complete understanding of how PCBs impair neurological development in the womb and early in life, but emerging evidence suggests that the ability of PCBs to cause brain damage stems in part from disruption to another component of the endocrine system, thyroid hormones.

Extensive research on the developing brain and nervous system has found that thyroid hormones help orchestrate the elaborate step by step process that is required for normal brain development. As touched on in Chapter 3, these hormones stimulate the proliferation of nerve cells and later guide the orderly migration of nerve cells to appropriate areas of the brain. The brain and nervous system, like other parts of the body, pass through critical periods during their development both in the womb and in the first two years of life. When thyroid levels are too high or too low, this development process will go awry and permanent damage will result, which can range from mental retardation to more subtle behavioral disorders and learning disabilities. The precise nature of the damage done by abnormal thyroid levels will depend on the timing and the extent of the disruption.

It has long been recognized that acute thyroid deficiency during pregnancy can cause profound mental retardation, but thyroid researcher Susan Porterfield, an endocrinologist at the Medical College of Georgia, notes that few have considered the more subtle effects of less severe thyroid disruption during the development of the brain and nervous system-disruption that can occur naturally or be the result of hormone disrupting chemicals in the environment.

PCBs and dioxin affect the thyroid system in diverse, complex, and as yet incompletely understood ways. Some analyses indicate they may mimic or block normal hormone action perhaps by binding to the thyroid receptor. Other data suggest they may even increase the number of receptors present to receive the hormone signals. They also seem to act particularly on T4, the form of thyroid hormone that is critical to prenatal brain development. Researchers Daniel Ness and Susan Schantz of the University of Illinois have established that two PCBs commonly found in human tissue and breast milk-PCB 118 and PCB 153-reduce T4 levels in rats exposed prenatally. These compounds also compete more powerfully than natural hormones for binding to a carrier protein called transthyretin, which transports T4 into brain cells.

In a June 1994 article in the journal Environmental Health Perspectives, Porterfield outlined her theory that "very low levels" of PCBs and dioxins-levels well below those generally recognized as toxic- can alter thyroid function in the mother and the unborn baby and thereby impair neurological development. Like Sharpe and Skakkebaek, Porterfield cites evidence showing that skewed hormone levels in the womb can cause permanent damage-in this case, learning disabilities, attention problems, and hyperactivity.

The emerging evidence linking PCBs to thyroid disruption and neurological damage is especially worrisome because PCBs are a persistent, ubiquitous contaminant whose levels are not decreasing significantly in human tissue even though most of the industrial countries stopped making them more than a decade ago. In the former Soviet Union, production of PCBs did not stop until 1990.

The most extensive data on neurological effects concern PCBs, but it is important to stress that PCBs are not by any means the only culprit. Many other synthetic chemicals act on thyroid hormones as well, adding to the concern. The thyroid system is one of the most frequent targets for synthetic chemicals, according to Linda Birnbaum, who heads the environmental toxicology division at the U.S. Environmental Protection Agency's Health Effects Research Laboratory. With the possibility for multiple assaults on the thyroid system, the hazards to the developing brain may be considerable. Based on the concentrations in breast milk fat of PCBs alone, some have estimated that at least 5 percent of babies in the United States are exposed to sufficient levels of contaminants to cause neurological impairment.

 

 

 

 

 

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