of Medicine (NEJM) that again called attention to the concept of “undue lead absorption” as a stage before overt lead poisoning and identified lead in dust and soil as a problem. She argued that the existing criteria, even for undue lead absorption, might still be too high. She pointed to numerous studies that led her to conclude that “the upper limit of normal [i.e., “safe”] should be no higher than 40 µg per 100 ml and may actually be lower.”24 After a review of the shocking statistics from New York City, Newark, New Haven, Philadelphia, Washington, D.C., Baltimore, and Chicago, among other cities, revealing the number of children who had blood lead levels above 40 µg/dl, she concluded that “in magnitude the problem of undue absorption of lead among children living in old neighborhoods is matched by few, if any, other pediatric public health problems.”25
This was a truly stunning conclusion. At a time when measles, mumps, and rubella still posed a substantial threat to American children, a handful of public health professionals like Lin-Fu were identifying possibly a worse scourge. The NEJM article had a profound impact, she recalls, because she had “raised the question of subclinical neurological damage,” such as behavioral problems, learning disabilities, reduced IQ, and perceptual difficulties26—“subclinical” at the time meaning merely that physicians of that era defined such symptoms as psychological or behavioral issues, not medical or biological ones.
THE TOOTH-FAIRY PROJECT
Jane Lin-Fu’s analysis built on the findings of the blood lead surveillance programs that local public health departments across the country were implementing in the late 1960s and early 1970s. These programs were uncovering a huge number of children with blood lead levels above 40 µg/dl but who did not show overt clinical symptoms. Were the levels that were being found dangerous to the health of the child? What did these elevated blood lead levels mean for the neurological development of school-age children? Was there a way to estimate whether or not such children had experienced chronic, long-term exposure to lead? And if these children had experienced such chronic exposure, what impact had that had on their development?
These issues would take on special importance with the 1972 publication in Nature of a landmark article whose primary author, Herbert Needleman, a forty-one-year-old professor of pediatrics at the University of Pennsylvania, would become a lightning rod for the growing controversy over “subclinical” effects of lead on children. In the article, Needleman—along with his coauthors Irving Shapiro, a University of Pennsylvania assistant professor of dentistry, and Orhan Tuncay—began to develop a methodology and conceptual framework that would transform lead research by the end of the decade. In the early 1970s, blood lead levels were the diagnostic tool for defining lead poisoning. Without an elevated blood lead level, still commonly defined by most local health departments as more than 60 µg/dl, physicians generally assumed that a child was not poisoned. But Needleman’s study raised the question of whether blood lead levels alone were an adequate measure of safety or harm. As Needleman and his associates explained, “Because elevations in blood lead are transitory, and decline once ingestion has stopped, blood lead levels are unsatisfactory indices of earlier exposure” and therefore inadequate for determining long-term exposure.27 Or as Needleman later explained, testing for blood lead “represents a single static measurement of a number of dynamic processes.”28
Needleman drew upon a method perfected by Barry Commoner, the environmental scientist and peace activist who, in the 1950s, had raised public awareness of the dangers of strontium 90, a by-product of atomic testing. At the height of the Cold War, as both the United States and the Soviet Union raced to develop ever more powerful atomic weapons, hydrogen bombs in particular, huge demonstration detonations had become commonplace. This testing released radioactive materials into the atmosphere that eventually settled to earth and were absorbed by children through ingestion of milk and other foods. Commoner and Anthony Mazzocchi, then a young organizer and official for the Oil, Chemical and Atomic Workers Union on Long Island, collected baby teeth to show that the radioactive material released in the distant testing grounds in Utah, the Pacific Islands, and Siberia soon became, in the words of the New York Times, “a lifelong component of the teeth and skeleton.”29 Needleman and his colleagues knew that calcified tissue, such as that found in baby teeth, likewise stored lead, and they hit upon the idea of using that as a means of measuring long-term exposure.
In a research effort whimsically called the Philadelphia Tooth Fairy Project, Needleman and his team allied with dentists in Philadelphia’s “lead belt” to collect 69 baby teeth. In addition, they collected 40 teeth from suburban dentists. The results of their analysis were stark and startling: children living in poor urban communities had nearly five times the levels of lead compared to those living in the suburbs.30
Lead researchers had always known that lead in the blood was only a snapshot of a child’s recent exposures to the toxic metal. They also knew that some of the lead that children ingested accumulated in their bones and remained there for years, even decades. There was little consensus about—and there had been no way of accurately measuring—the impact of lead that had accumulated over time, however. It was impossible to routinely do bone biopsies of living children with suspected, but asymptomatic, cases of lead exposure; and X-rays merely showed the presence, not the amount, of lead. Needleman’s new methodology promised to provide some answers to the scientific conundrum of whether or not children’s long-term exposure to lead was correlated with damage. The complexity and the terrifying dimensions of the lead pollution issue were, with Needleman’s research, to soon become more apparent to the research community. No longer would scientists, physicians, and the public health community be able to take comfort in focusing only on the acute impacts of lead as measured by elevated blood lead levels.
Needleman’s continuing work would eventually set off a firestorm of opposition from the lead industry. In October 1972, Needleman traveled to Amsterdam to present a paper at a symposium on environmental health aspects of lead that was sponsored by the recently established Environmental Protection Agency and the Commission of European Communities.31 This meeting, Needleman later told journalist Lydia Denworth, was where he realized that powerful interests were going to oppose his scientific findings: “I woke up to the fact that it wasn’t just that the truth will out.”32 The meeting brought together hundreds of representatives from twenty-one countries, including government officials, people from private industry, and independent research scientists. Forty-two came from the United States, of whom eighteen were industry representatives, some of whom took a very dim view of Needleman’s work.
Needleman began his talk by discussing the difficult problem that relatively low-level lead exposure presented for researchers and clinicians alike. Lead poisoning challenged the older paradigm of what constituted health and disease. Lead poisoning was unlike acute infectious diseases that ultimately resolved themselves or resulted in observable, permanent damage. Unlike polio, for example, which left children (many of its victims), visibly disabled, children who were lead poisoned looked normal, exhibiting in all but extreme cases neurological, emotional, cognitive, and behavioral problems that initially might be easily overlooked. While IQ loss, dyslexia, hyperactivity, and behavioral problems could tragically change the direction and prospects of lead poisoning’s victims, these symptoms were not commonly ascribed to the effects of lead. Except in acute cases of lead poisoning, it was also unlike other recent health crises. “When an agent produces dramatic symptoms, the establishment” of the cause, was “relatively easy.” This was the case with thalidomide, a sedative prescribed in the late 1950s for women suffering from morning sickness that was found to cause birth defects. “Had Thalidomide produced mental retardation rather than phocomelia [the underdevelopment of various parts of the face, limbs, and body resulting in severe disfigurement], it would probably still be sold in Europe and the United States.”33
Needleman was among the first to suggest that the effects of lead poisoning could be thought of as “a family of curves,” starting with subtle biological change “at the lowest levels”; continuing with irritability, awkward gait, and fevers in the middle levels and comas and convulsions near the top; “and
