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.
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,
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.
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.
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.