Joseph G. Hollowell

Reported biomedical causes and associated medical conditions for mental retardation among 10-year-old children, metropolitan Atlanta, 1985 to 1987

This report describes biomedical causes of mental retardation(MR) among school‐age children and associated medical conditions in children for whom no cause was reported. This study involved 715,10‐year‐old children with MR (intelligence quotient [IQ] 70 or less) born between 1975 and 1977. We determined biomedical causes of MR using a hierarchical approach based on the timing of the event (i.e. prenatal, perinatal, or postneonatal). Among, children with no identified biomedical cause the occurrence of associated medical conditions was examined. No reported biomedical cause could be found in 78% of children with MR (87% mild, IQ 50 to 70; 57% severe, IQ<50). Prenatal causes were present in 12%, perinatal causes in 6%, and postneonatal causes in 4%. On the basis of these findings it was concluded that intensive use of public health prevention strategies can reduce the number of children who receive a diagnosis of MR.

Revision of the International Classification of Impairments, Disabilities, and Handicaps: Developmental issues

Variability in approaches to define and classify disability has constituted persistent problems in documenting the epidemiology of disability and providing appropriate services. The major institutions of health care, mental health, and welfare often have separate systems of classification and terminology related to defining eligibility for programs and funding for services. In 1980, the International Classification of Impairments, Disabilities and Handicaps-ICIDH was published by the World Health Organization as a companion document of the International Classification of Disease to document the consequences of illness or injury. Current problems concerning the classification of childhood disability in health, education, and related services have resulted in growing interest in the revision of the ICIDH as a classification tool. The strengths and limitations of the ICIDH are examined in general, as well as with specific reference to its ability to document the nature and epidemiology of childhood disability. This paper (1) describes the ICIDH taxonomy and representative contributions; (2) reviews issues and concerns contributing to its revision; (3) summarizes changes in the revised ICIDH2 draft document, and (4) identifies issues of particular relevance to children and public health applications.

Use of Inductively Coupled Plasma Mass Spectrometry to Measure Urinary Iodine in NHANES 2000: Comparison with Previous Method

Urinary iodine (UI) concentrations directly reflect dietary iodine intake and consequently test biochemical assessment of the iodine status worldwide (1).nnThe Iodine Laboratory of the Division of Laboratory Sciences at the National Center for Environmental Health, CDC, measured the UI content of specimens as part of the National Health and Nutrition Examination Survey (NHANES) 2000 and will measure UI in the US population through future NHANES analyses, using inductively coupled plasma mass spectrometry (ICP-MS). In this report, we describe the ICP-MS laboratory method and compare that method with the established Sandell–Kolthoff (S-K) spectrophotometric method used in NHANES III.nnThe ICP-MS method described previously (2) was modified for use in NHANES 2000 by adding alkaline diluents and rinses to measure UI as follows: urine samples and the urine iodide calibrator solutions were prepared just before analysis by dilution (1:49; 50 μL of sample/calibrator plus 2450 μL of diluent) with an aqueous solution of 10 mL/L tetramethylammonium hydroxide containing 10 μg/L tellurium as an internal standard. A peristaltic pump introduced the diluted samples into the spray chamber with an argon stream. The I+ and Te+ ions were measured at m/z 127 and 130, respectively (3). The diluent used to make the intermediate working calibrators was 1.0 g of analytical-reagent-grade sodium thiosulfate (Na2S2O3) dissolved in 1000 mL of 18 MΩ · cm ultrapure water. (The water used for all dilutions and rinses in the ICP-MS method is ultrapure 18 MΩ · cm water; Millipore Corporation.) The wash solution was an aqueous solution of 1 mL/L Triton X-100 and 10 mL/L tetramethylammonium hydroxide. This solution was …

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 pre- and 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, Program Against 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.

Chernobyl and iodine deficiency in the Russian Federation: an environmental disaster leading to a public health opportunity.

The Chernobyl nuclear disaster of April 26, 1986, triggered a chain of devastating events that later included an unexpected increase in childhood thyroid cancer and evidence of iodine deficiency (ID) in Russia. For the Russian people the Chernobyl event had profound psychological impacts, provoking anxiety about nuclear technology and mistrust of governmental control efforts. Frequently in public health a crisis is required to create the political will to manage longstanding problems, and public health officials must rapidly mobilize to take advantage of the opportunity. In this case, ID, previously not seen as a problem in Russia, was recognized to be potentially serious, and the Russian Federation, assisted by the catalytic binational effort of the U.S.-Russian Joint Commission on Economic and Technological Cooperation (Gore-Chernomyrdin Commission (GCC)) established a model salt iodization policy, developed a planning process, and implemented a program to prevent ID through a systematic approach that included the people, government, and private groups using open communication, dissemination of the findings, and action plans. By 1999, political will had been mobilized and over 20% of the nations salt was being iodized, up from about 1% in 1996. Universal iodization of salt was not a specific objective of the GCC; however, the increasing availability of iodized salt is leading to the elimination of ID, which is now a political goal in Russia. The full realization of this goal will require more time for education, marketing, and possibly legislative action.