During the years 1952 to 1954 in Baltimore, Maryland, 197 lead-exposed children were studied, including 89 with acute encephalopathy. Of those with acute encephalopathy, 4 children died and 23 had severe sequelae such as severe mental retardation, behavior disorder, or recurrent convulsions. These poisonings were caused by the ingestion of lead-based paint. Strikingly, even ingestion of very small quantities of paint flakes was associated with serious illness. Illness onset was most often in the summer season. Lead exposure in children who were originally used as unexposed control subjects was found to be significant as well, indicating that lead exposure as a child health problem is much more extensive than heretofore thought to exist. The only adequate protective measure is removal of lead from the child's environment.
Healthy children need healthy environments, and everyone benefits when the overall environment is made healthy for our children. In the earlier years of Pediatrics, the subject of children's environmental health was addressed infrequently, except through committee statements. As is true with all of environmental health, early concerns focused on the environment's role in the spread and prevention of infectious disease.
The most remarkable pediatric environmental health success during the existence of Pediatrics is the approaching triumph over childhood lead poisoning in the United States. Although lead harms all biological systems, its most pernicious effects are on the developing brains of children.1
Lead poisoning prevention has been the centerpiece of environmental protection efforts related to children. For this reason, it is appropriate to choose as the seminal article on children and the environment one that relates to childhood lead poisoning. The saturation of the environment by lead during the era of the baby boom was astonishing. Paint in most homes in the late 1940s was, in essence, a crust of lead. The solder of water pipes and food cans, even those containing infant formula, was lead. Many consumer products, including toys, were made or painted with lead. Most profound, each month millions of pounds of lead, in highly absorbable microscopic particles, blasted from automobile exhausts in every corner of the nation. In the 1960s many inner city hospitals had large numbers of comatose and convulsing children with lead poisoning, with fatality rates of 5% to 28%.2 One 1972 survey of inner city children living in Rochester, NY, documented blood lead levels as high as those among children living near smelters.3
Over the last 40 years, lead has been removed from all these sources, and the average blood lead level of America's children has fallen to 2.7 mcg/dL. Over the same period, the Centers for Disease Control and Prevention's level of concern for lead toxicity has fallen from 60 to 10 mcg/dL because of increasing recognition that lead levels once thought to be modest had subtle but long-lasting effects on the brain.4 Despite much progress, the effort to remove lead from children's environments is not yet completed; ∼1 million children remain with elevated lead levels in the United States.5 Of interest, the risk factors for having an elevated blood lead level are the same today as they were when Drs Chisholm and Harrison wrote their article. Risk remains highest for children who are poor, African-American, and who live in older housing, especially in larger cities.5
The importance of this paper from 1956 is that it was the first inPediatrics to document systematically that the child's environment was the most important risk factor for childhood lead poisoning. Important also is that the first author, Dr Julian Chisholm of Johns Hopkins in Baltimore, MD, is one of the leaders in the study of childhood lead poisoning.
Drs Chisholm and Harrison described lucidly the clinical picture of childhood lead poisoning, the seasonal onset of acute encephalopathy, and the sequelae of lead poisoning, both neurologic and cognitive. As clinician researchers, they were interested in the treatment of acute poisoning and recorded the excretion of lead by children who had lead poisoning and those who did not. They remarked that the children under study had higher lead excretion than even exposed lead industry workers. They found that chelation of lead from intoxicated children could not prevent the toxic effects of prolonged absorption. They demonstrated the importance of environmental risk factors and that ingestion of just a few tiny paint chips per day was enough to intoxicate a child. Lead, especially in the form of flecks of paint chips, saturated the environment of these children, and the authors stated, “Such intense exposure … constitutes a public health problem which may be more extensive than has heretofore been thought to exist.” They asserted that the child's environment was more important than either social or behavioral factors, and concluded that the most important interventions were preventive and environmental, stating that “removal of lead from the child's environment is the only adequate protective measure”.
Chisholm and Harrison demonstrated that households in which lead-poisoned children lived were more likely to contain other lead-exposed children. They showed that checking the housemates of children in the hospital identified other poisoned children. Their recognition of the importance of chronic or repeated lead exposure in increasing the risk for neurologic sequelae also was important. Finally, they asserted that management of lead-poisoned children must include nonmedical partners able to evaluate and help manage housing and social problems.
Childhood lead poisoning is a complex disease that requires a team response: environmental, social, and medical. Lead must be removed from the child's environment; this is the rationale for today's environmental control programs established around the country. This article was prophetic in identifying housing as the critical children's environmental health issue.
Much of the report has stood the test of time, including its descriptive epidemiology, which described that 1- to 3-year-old children were at the highest risk, and that numbers of cases peak in the summer. Some assertions made in the report have now been superseded. For example, research yet to come demonstrated that there are no normal lead levels; the less lead in the developing brain the better.6,7 This 1956 article also did not recognize that severely poisoned children were left with lifelong sequelae,8 a reflection of the limited neurocognitive testing instruments available at the time.
The advances in childhood lead poisoning prevention have come about because of efforts from across all of society. None of this would have happened, however, without the contributions of clinicians who identified this disease and described its acute and long-term damage, even when confronted with personal attack. The importance of this work is now recognized worldwide; many countries are mandating the removal of lead from gasoline.
This article played a pivotal role in highlighting an issue of critical importance to children's health, coauthored by Julian Chisholm, who would go on to make other remarkable contributions as a researcher, teacher, and advocate for children. The article helped alert society to the tragic consequences of lead poisoning and the urgent need to remove lead from the environment of all children.
- ↵Lin-Fu JS. Historical perspective on health effects of lead. In: Mahaffey K, ed. Dietary and Environmental Lead: Human Health Effects. New York, NY: Elsevier Science Publications; 1085:43–63
- ↵Centers for Disease Control and Prevention. Preventing lead poisoning in young children: a statement by the Centers for Disease Control. Atlanta, GA: US Dept of Health and Human Services, Public Health Service; 1991
- Copyright © 1998 American Academy of Pediatrics