Teratogen update: iodine deficiency, a community teratogen.

In the last decade, iodine deficiency disorders (IDD) have become recognized as the most common preventable cause of mental retardation worldwide. Iodine deficiency interferes severely with prenatal and postnatal growth and neurologic development of individuals. It has condemned tens of millions of children to cretinism—characterized by mental and growth retardation, rigid spastic motor disorders, deaf mutism, and severe hypothyroidism—and hundreds of millions of children to milder degrees of mental and physical impairments. Accompanying effects include increased rates of congenital anomalies, fetal wastage, infant mortality, goiter, and hypothyroidism in children and adults. Endemic cretinism has been classically divided into two types: a chronic neurological disorder and a condition with myxedema and severe hypothyroidism. Recent studies have shown considerable overlap in the findings of these two types, which are now thought to have a common etiology differing primarily by the timing and severity of the preand postnatal deficiency of iodine and maternal thyroxine. The severity of iodine deficiency and hypothyroidism in the mother during early and midgestation is related to the severity of the neural damage in the fetus. The most logical intervention for a community or population is the introduction of iodine prophylaxis. Although salt iodization is technically straightforward, community leadership is essential to any effort. The mobilization of global efforts through WHO, UNICEF, ProgramAgainst Micronutrient Malnutrition (PAMM), and International Council for Control of Iodine Deficiency Disorders (ICCIDD) since 1990 has led to goals to eliminate new cases of IDD by the year 2000. Most countries at great risk for IDD have met or are close to meeting the middecade goal of having iodized salt for 90% of households. This provisional success indicates that the goal of eliminating new IDD cases by the year 2000 may be achieved.