Research has shown that children exposed to common environmental toxins like dioxin and polychlorinated biphenyls (PCBs) prenatally and during infancy can suffer behavioral, learning and memory problems. A University of Maryland School of Medicine psychiatry professor now suggests that the underlying mechanism may be disruption of the normal action of thyroid hormone.
In the January issue of the scientific journal Toxicology and Industrial Health, Dr. Peter Hauser and colleagues summarize recent studies that suggest links between perinatal exposure to dioxin-like substances and developmental abnomalities in learning and attention. They propose that the genetic condition known as resistance to thyroid hormone (RTH) may be a useful model for further study of the disruptive effects of dioxin and PCBs on brain development.
Hauser is professor of psychiatry at the UM School of Medicine and chief of psychiatry at the Baltimore Veterans Affairs Medical Center. Co-authors are Drs. J. Michael McMillin and Vinod S. Bhatara of the University of South Dakota School of Medicine.
Thyroid hormone plays an essential role in prenatal brain growth and development, as well as in normal behavioral and intellectual development. Even moderate impairment of thyroid hormone function has been associated with various problems in behavioral and intellectual development, and certain thyroid diseases such as RTH are associated with attention deficit hyperactivity disorder (ADD or ADHD) and language disorders.
"Optimal amounts of thyroid hormone appear to be of vital importance for central nervous system development and maturation during a critical period which begins in utero and continues in humans for approximately the first two years after birth," Hauser said.
During the first 12 weeks of pregnancy, thyroid hormone from the mother is transported through the placenta, where it affects fetal brainstem and brain-cell development. Through the remainder of pregnancy, both maternal and fetal thyroid hormone affect brain and central nervous system development.
"Major neurodevelopmental events occurring in this period are exquisitely sensitive to thyroid hormones," Hauser said.
Studies of adults exposed to dioxin and PCBs show no marked neurological effects. But numerous studies in humans and animals show that perinatal exposure frequently impairs brain and central nervous system development. Problems found include delayed speech and language development, slow development of reflexes and complex movements like walking, hyperactivity, and learning disabilities.
"Human and animal studies have demonstrated that exposure to dioxin-like compounds can alter thyroid hormone function and produce neurobehavioral changes, but it remains to be definitively established that changes in thyroid function are responsible for the neurobehavioral effects," said Hauser.
Since the neurological and behavioral abnormalities seen in humans who have been exposed in utero or infancy to dioxin-like chemicals are similar to those seen in people suffering from resistance to thyroid hormone (RTH), Hauser called for new studies that contrast RTH with perinatal exposure to dioxin and PCBs.
"Such studies may provide new insights into the basic pathogenesis of developmental neurotoxicity following exposure to thyroid-disrupting synthetic compounds and may provide guidance for treatment and prevention," he said.
Hauser and colleagues’ research was funded by the University of Maryland School of Medicine and the American Thyroid Association.
Materials provided by University Of Maryland, Baltimore. Note: Content may be edited for style and length.
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