LITMIR.BIZ

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give cars more power. With the dramatic growth of this vast industry, every American child, parent, and neighbor began to systematically incorporate into their bodies a toxic heavy metal that was already known to be poisoning workers in the United States and elsewhere.

      For centuries, and particularly with the Industrial Revolution, lead had been causing workers in foundries, smelters, paint factories, and other industries to suffer severe, sometimes fatal neurological damage. By the 1920s, children as well were facing a special threat from the very rooms they lived in every day. Paint, the seemingly innocuous wall covering that replaced wallpaper as the most desirable room decoration in the early twentieth century, contained huge amounts of this deadly material. Up to 70 percent of a can of paint in the first half of the century was composed of lead pigments. Such paint was aggressively marketed as the covering of choice to millions of young families through jingles, advertisements, and even paint books for children, who were told, for example, “This famous Dutch Boy Lead of mine can make this playroom fairly shine.”¹¹

      The vast expansion of America’s cities fueled growing use of lead paint as a convenience of modern American life, which also fostered competition among various paint manufacturers eager to gain new sales and capitalize on potential profits. The paint companies could have manufactured their products without lead—zinc-based paints (promoted as safe and nontoxic because they were “lead free”) had been on the market as early as 1900, and by the 1930s titanium pigments were available as well. Instead, the lead industry chose to run massive marketing and promotion campaigns all through the first half of the twentieth century despite their knowledge that lead paint was causing children to go into comas, suffer convulsions, and die.¹² The result was a major public health disaster. By the middle decades of the century, millions of children were suffering the effects of acute or chronic lead exposure, and tens of thousands of children had died.¹³ Lead was by then certainly among the most prevalent, if not the most well-known, of the threats to children.

      

      The Kennedy Krieger Institute had been identifying such lead-poisoned children and treating them for over a half century when researchers there embarked in 1991 on what became its controversial study.¹⁴ Baltimore, and Johns Hopkins University in particular, had been at the center of work on childhood lead poisoning even longer, for almost a century.¹⁵ Over this period, the city had made some of the more innovative attempts to address what has proven to be one of the nation’s most intractable environmental problems. In the 1930s Baltimore’s health commissioner identified lead paint as a major source of injury to children, and since the 1950s Johns Hopkins had numbered among its faculty the foremost lead researchers in the nation, including Julian Chisolm, perhaps the preeminent university lead researcher of the middle decades of the twentieth century—and the co-principal investigator for the KKI study. The irony of this history is unmistakable. Here was the premier center for the study of lead poisoning, located in the virtual heart of the country’s lead poisoning epidemic, at the eye of a storm over whether or not children were being used, as the Maryland Court of Appeals ultimately opined, as “canaries in the mines”¹⁶ and “guinea pigs.”¹⁷

      Fairly typical of the thousands of children that Johns Hopkins had sought to help before the 1960s, when children living in poorly maintained slum housing suffered from convulsions after ingesting lead paint, was John T., aged nine months, who was brought by his distraught parents to the Harriet Lane Home of the Johns Hopkins Hospital in February 1940.¹⁸ John was a well-nourished, playful, and cooperative child, with no history of developmental problems, according to the admitting nurse. John’s father was well educated, having spent three years at a theological seminary. He had also trained as an entertainer, but a back injury had incapacitated him and he had gone on relief, receiving fifty-six dollars a month to support his family. Despite their meager income, their home was well maintained and “quite attractively furnished,” the visiting social service worker reported.¹⁹

      John was admitted to the hospital because he had developed an ear infection, but that was easily treated; his appetite was good and he slept well. The medical record indicated that John had been breast-fed for six of his first nine months. He was soon eating cereals; started on spinach, string beans, and other vegetables; and given soft-boiled eggs. In his short life he had never suffered from nausea or vomiting. The record reported a happy, healthy infant from a good home who “held up his head at three months; sat up at six months; had first teeth at seven months,” and at month nine was able to walk around holding on to objects and walls. “This baby behaves well,” said the record. “No problem. Keeps himself entertained all day.” He had suffered an attack of chicken pox but had recovered well. In a matter of two days his ear infection seemed to clear up and he was sent back home to 1023 North Caroline Street, a three-story row house just north of the medical center, to rejoin his four other siblings, who ranged in age from two to six years. This healthy child had everything to look forward to.

      In the ensuing months John returned periodically to the clinic for treatment of his chronic earaches, but by the time he was two years old he had developed symptoms that were not at all routine. In May 1941 his parents rushed him to the hospital. A few hours earlier, he had “bent over to the left and couldn’t straighten up,” they told the admitting nurse, and since that time he had “been acting ‘crazy-like.’” John had been “eating plaster,” they said, and the previous day he had eaten “some paint.” The nurse summed up what she had observed: “This is a fairly well-nourished and developed two year old colored boy who is crying and is excitable.” At the hospital he “fell to the left side when he tried to walk, and he reeled around to the left. He didn’t respond to his name or questions.” The hospital raised the possibility that John suffered from lead poisoning, encephalitis, and secondary anemia. He had apparently been eating plaster for the past six months, and his mother reported that “he has been eating paint that peels off from window sills.” The blood work showed 390 micrograms of lead per deciliter of blood—almost eighty times the level considered by the CDC to be dangerous for children seventy years later²⁰ and at the time clearly a cause of acute poisoning. The social worker in charge of the case noted that “because the landlord refused to make any repairs in this home, the family pooled their money and bought some paint which they have used all over the home.” When told that paint from the windowsills was dangerous, his mother said she had not realized its danger and had “caught him on frequent occasions with a mouth full of paint chips.” She promised that in the future “she would make every effort to keep the child away from the paint.” She had “a large play pen and from now on the child [would] be kept there. It gives him adequate room to move about and have a good time,” the social worker wrote, “and will make it impossible to get to the window sill and eat more paint.”

      In mid-June 1941, after more than a month in the hospital, John’s symptoms subsided and he was sent back home. But two months later the mother was back at the social service department. In the words of the social worker, the family had “contacted the real estate agency several times about repair work but with no success”; there continued to be problems of “loose plaster throughout the home in spite of their efforts at repair.” The social worker contacted the health department, which promised to investigate the home conditions, but we know neither the results nor what befell John in subsequent years.

      What did and did not occur in response to the plight of John’s family is telling. At the time, Johns Hopkins was the lone institution and Baltimore the lone city in the country that was systematically trying to identify and treat large numbers of children affected by the increasing tonnage of lead polluting the nation’s housing. Baltimore and Hopkins had been the epicenter of this issue ever since the area’s rapid growth at the turn of the century had created a huge housing boom and, with it, the use of lead-based paint throughout the central city. The first American case of poisoning due to lead paint ingestion was also documented here, in 1914, by Henry Thomas and Kenneth Blackfan at the very same Harriet Lane Home where John was treated. And Baltimore’s Department of Health was the first local health agency to mount a campaign to protect a city’s children from the effects of lead. In fact, in the 1930s it used the new medium of radio to broadcast public service announcements warning its residents about lead’s dangers: “Every year there are admitted to the hospitals of Baltimore a number of children with

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