Abstract
Over the past fifteen years, knowledge of the spectrum of lead neurotoxicity has increased dramatically. Since 1979, when Needleman and colleagues1 showed that deciduous tooth lead levels were inversely related to intellectual performance and behavior in school-age children, many well-designed epidemiological studies have confirmed that low-level, subclinical lead exposure in early life is associated with decrements in childhood cognitive performance.2 These human findings cohere with substantial primate evidence, which consistently demonstrates measurable and long-lasting neurodevelopmental deficits from exposure to low levels of lead.3 In response to compelling evidence of neurotoxicity from low-level lead exposure, the United States Centers for Disease Control (CDC) issued a revised lead statement—Preventing Lead Poisoning in Young Children—in October 1991.4
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