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“to survey the scope of the lead-paint hazard and establish methods for abatement.”¹⁹ More broadly, the law set in motion surveillance of the lead problem nationally.²⁰ Thus, as early as 1970, lead paint abatement was considered essential to any attempt to deal with the lead problem. But it quickly became clear that the funds to address true removal would not be forthcoming anytime soon, fulfilling the prophesy of the Lead Industries Association that lead pollution would plague the country for the indeterminate future.

      The administration and Congress initially refused to appropriate or even request the funds to implement lead-abatement or poisoning-prevention programs that were authorized by the Ryan-Kennedy Bill. As reporter Jack Newfield wrote in June 1971, six months after the law was passed, even though the appropriations bill for that fiscal year “included funds for every special interest: $3.5 million for dairy and beekeeper indemnity; . . . [and] $15 million for highway beautification . . . [there was] not one cent for lead poisoning.²¹ The New York Times reported that as the cities “waited . . . the politics of embarrassment began. . . . The Administration asked for $2 million, which was raised to $5 million in the House and $15 million in the Senate, before the $7.5 million was agreed on in conference.” Later that year, on August 14, 1971, Congress finally appropriated the agreed-upon amount.²²

      In its account of the politics of appropriations for lead poisoning, the Times identified a fundamental conflict embodied in the act and in lead-poisoning prevention programs in general: Should “prevention” measures apply only to children who were already poisoned? Or should abatement of lead-infested houses take place before children were damaged? This raised a fundamental question that would plague lead specialists and, the public health profession and society more broadly: Were children in effect their own “canaries in the mine”? As the Times put it, “what constitutes prevention . . . remains unsolved among public health practitioners. The few lead poisoning programs currently in operation around the country all look for children with high levels of lead in their blood and then clean up the environment that poisoned them.” The newspaper noted that many in public health wanted a true prevention program, “a systematic clean-up of housing known to contain lead before children can ingest the paint.” In the end, such a systematic program of detoxifying the housing stock might be slow, but it would be “more useful and less costly.” The New York City Health Department had found that “93 percent of 2600 reported cases [of lead poisoning] last year could be traced to housing”; but in New York, as in Chicago, Baltimore, and other cities, “repair is only authorized in the dwelling unit in which the child has been poisoned even though other apartments in the same building may be equally hazardous.”²³

      Meanwhile, the magnitude of the problem was becoming increasingly apparent as damage was found to be occurring to children at lesser levels of contamination than previously realized. In March 1972, Lin-Fu published an influential article in the New England Journal 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

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