ABSTRACT
It was in Australia in the 1890s, two millennia after lead was recognized as an adult
neurotoxicant, that childhood lead poisoning was first described (1). For the next half-
century, it was conceptualized largely as a clinical intoxication that was simply “present” or
“absent.” Moreover, the intoxication was thought to have no lasting impact if a child did not
become encephalopathic, which tends to occur at blood lead levels greater than 100 mg/dL. The observations of Byers and Lord (2) posed the first major challenge to this view. In this
case series, many of the lead poisoned children who presented without signs of encepha-
lopathy nevertheless suffered significant, enduring behavioral and intellectual problems
that interfered substantially with their well-being. This suggested that lead poisoning is
better characterized as a continuum than as a dichotomy, with subtler forms of neurological
deficit occurring among children with lead exposures that do not produce frank toxicity.
