the country, large city health departments were pressed by community groups and concerned professionals to expand surveillance efforts and screening programs, which brought greater awareness of the extent of lead exposures and concern that Clair Patterson and Harriet Hardy were accurate in arguing that lead poisoning was a much more serious problem than previously assumed. According to one government expert, by the late 1960s several large cities, including Chicago and New York, “reported that 25 to 45 percent of one- to six-year-old children from high-risk areas had blood lead levels exceeding 40 µg per 100 ml.”79
As doctors became more alert to the possibility of lead poisoning, the numbers of those acknowledged to be affected naturally increased. But the fatality rate didn’t. In Chicago, in 1966, for example, a study of more than 60,000 children showed “a marked rise in cases reported [compared to the 1950s] and a sharp decrease in fatality rate.”80 In New York, like Chicago, the fatality rate among those diagnosed with lead poisoning declined from 27 percent in the 1950s to 1.4 percent in 1964.81 Such drops in the fatality percentage were in part a function of increased surveillance and a lower threshold used to trigger a diagnosis of lead poisoning, which increased the pool with which the percentage was calculated but not the fatalities. But beyond that, it was widespread use of chelating agents that was responsible for this remarkable decline. An early champion of chelation therapy was J. Julian Chisolm, who would years later be the co-principal investigator of the KKI study so excoriated by the Maryland Court of Appeals.
As a young physician in the 1950s, trained at Johns Hopkins and at Princeton before that, Chisolm was in his generation almost unique in his ongoing professional focus on lead poisoning, particularly among African American children. In the early 1950s he received a fellowship to study the breadth of lead poisoning among Baltimore’s children. He visited homes, collecting stool samples of young children to analyze their lead content, and found that the City had been grossly underestimating the extent of the problem. He recalled that his “first findings . . . were that children who ingested paint were getting more lead than even heavily exposed industrial workers.”82
FIGURE 4.J. Julian Chisolm examining a child, ca. 1972. Chisolm was one of the early pioneers who called attention to the lead-poisoning epidemic, and throughout his life he treated thousands of lead-poisoned children in Baltimore. Source: Baltimore Sun, March 14, 1972, reprinted with permission.
Chisolm’s own background, perhaps, stimulated his commitment to and concern for African American children. Ironically, he came from a long line of southerners whose roots were in the South Carolina planter class. His great-great-great uncle, also named J. Julian Chisolm, was the leading surgeon for the Confederacy during the Civil War and author of the primary text for Confederate army surgeons.83 That Chisolm moved to Baltimore after the Civil War, established the Presbyterian Eye, Ear and Throat Charity Hospital, and became professor of ophthalmology and dean at the University of Maryland School of Medicine in Baltimore.84 J. Julian Chisolm Sr. (our J. Julian Chisolm’s father), himself the son of a Presbyterian minister who presided over a Natchez, Mississippi, segregated congregation of African American and white parishioners, received his medical degree from Johns Hopkins early in the twentieth century and taught at the medical school there for many years.85
J. Julian Chisolm Jr., who died in 2001, was a tall, large man with “a round face and sort of wispy hair that wasn’t very well combed,” according to Ellen Silbergeld, his student and protégé. He was mild mannered “in a kind of old Maryland gentleman way,” she remembers, and he “always wore a bow tie as the pediatricians in his day did,” so that young children couldn’t grab his tie. He could also be “very acerbic” to those who denied the importance of issues he cared deeply about. That the poisoning of African American children was one of these, Silbergeld said, “probably inhibited his promotion at Hopkins . . . to full professor until he was almost dead.” His commitment to the children he treated from the neighborhood around Hopkins was unquestioned by his students and colleagues. He once told Silbergeld that he saw racism inherent in the society’s lack of response to lead poisoning. “If this was a disease of white children,” he told her, “we would have done something about this a long time ago.” From these experiences came a life-long passion to address the effects of lead paint as the primary source of danger to children.86
Chisolm was working against the ingrained segregationist culture of Baltimore and Johns Hopkins at this time. Like other medical schools, Hopkins was an institution dominated by relatively wealthy, white, overwhelmingly male doctors and trustees. It was a “white enclave on a hill surrounded by” a largely poor African American community, recalls Connie Nathanson, now a professor of sociomedical sciences at Columbia, who worked in pediatrics at the Hopkins medical school from the late 1950s until 2002.87 In the postwar period, plans were developed for 178 garden apartments for African American families who were being displaced by the urban renewal project close to the Hopkins medical school campus. Those same plans included housing for residents and staff at the university. As social scientist Stephanie Farquhar documents, the “planned 178 garden apartments for blacks were never built . . . though the garden apartments for Hopkins married staff and the residence hall for Hopkins’ unmarried staff and students were.”88 Nathanson recalls that the “housing for residents and interns [was] surrounded by wire fencing that segregated it off” from the surrounding community.89
By 1969 the combined use of the two chelating agents, BAL and EDTA, according to Chisolm, “apparently reduce[d] the mortality from acute lead encephalopathy to 5%.” It was a pyrrhic victory, though, for “the incidence of severe, permanent brain damage among survivors of encephalopathy continues to be 25% or more,” he said. And “if survivors of an initial attack of acute lead encephalopathy are re-exposed to abnormal lead exposure the incidence of severe permanent brain damage is increased to virtually 100%.”90 Chisolm clearly understood the critical connection between treatment of children and the need to rehabilitate the housing where they lived. “The cornerstone of our current therapeutic program,” he argued, “is prompt termination of environmental exposure to lead: no child with an increased body burden of lead is ever returned to a leaded home.” Although it is not clear how often this was accomplished or who paid for this service, Chisolm wrote that after chelation therapy, children at Johns Hopkins clinics were either placed in suitable new housing or their homes were abated of lead. Chisolm understood that children having to be poisoned before remedial action was taken was both destructive for the child and expensive for society. “How much more intelligent it would be,” he commented, “to spend our effort and substance on the systematic elimination of environmental lead exposure associated with old dwellings. Were this to be done, childhood lead poisoning could be largely eradicated in the United States.”91 Although the solution was obvious, the means of attaining it were not. In the late 1960s there were, for example, thirty million housing units nationwide still in use that had been built before 1950; of these, at least 90 percent were polluted by lead.92
3Peeling the Onion
New Layers of the Lead Problem
The worth of the human brain is incalculable. The value we assign to it will be defined by the intensity with which we pursue or avoid the protection of its optimum development. Excess lead in the human environment is man-made and is, therefore, preventable by man.
HERBERT NEEDLEMAN, 1977
Prior to 1970 and the establishment of the Environmental Protection Agency, the federal government rarely regulated environmental toxins. But by the late 1960s and early 1970s, environmentalists and public health officials were advocating such regulation to protect the food supply and improve air and water quality. The Food and Drug Administration had begun to expand its role in regulating foods and additives after a weed killer, aminotriazole, feared as a carcinogen, was found
