in many countries continue to poison communities around the world. Industrial societies in the West may have significantly reduced the levels of new lead contamination, but the horror of lead poisoning here is hardly behind us, exposure coming from lead paint in hundreds of thousands of homes, in airborne particles from smelters and other sources and from contaminated soil, lead solder and pipes in city water systems, and some imported toys and trinkets. Over time, millions of children have been poisoned.
In the past, untold numbers of children suffered noticeably from irritability, loss of appetite, awkward gait, abdominal pain, and vomiting; many went into convulsions and comas, often leading to death. The level of exposure that results in such symptoms still occurs in some places. But today new concerns have arisen as researchers have found repeatedly that what a decade earlier was thought to be a “safe” level of lead in children’s bodies turned out to itself result in life-altering neurological and physiological damage. Even by the federal standard in place at the beginning of 2012 (10 μg/dl), more than a quarter of a million American children were victims of lead poisoning, a condition that almost a century ago was already considered with some accuracy as totally preventable. Later in 2012, the Centers for Disease Control (CDC) lowered the level of concern to 5 μg/dl, nearly doubling estimates of the number of possible victims.
The ongoing tragedy of lead poisoning rarely provokes the outrage one might expect, however. If this were meningitis, or even an outbreak of measles, lead poisoning would be the focus of concerted national action. In the 1950s, fewer than sixty thousand new cases of polio per year created a near panic among American parents and a national mobilization of vaccination campaigns that virtually wiped out the disease within a decade. At no point in the past hundred years has there been a similar national mobilization over lead despite its ubiquity and the havoc it can wreak.
For much of the twentieth century we have no systematic records telling us the number of children whose lives have been destroyed by lead. What we have known, as one researcher put it in the 1920s, is that “a child lives in a lead world.”10 By the 1920s, virtually every item a toddler touched had some amount of lead in or on it. Leaded toy soldiers and dolls, painted toys, beanbags, baseballs, fishing lures, and other equipment that were part of the new consumer economy of the time; the porcelain, pipes, and joints in the sparkling new kitchens and bathrooms of the expanding housing stock—all were made of or contained large amounts of lead. But more ominously and disastrously, lead became part of the air Americans breathed when, in 1923, lead was introduced into gasoline to 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
