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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 in cranberries just before the 1959 Thanksgiving holiday. Environmental activists and the broader public also joined together to press for greater regulation following publication of Rachel Carson’s Silent Spring in 1962, with its vivid account of the devastating effects of DDT and other pesticides on birds and other wildlife, and then the revelation in 1966 that PCBs and other chlorinated hydrocarbons were accumulating in animals—including Homo sapiens—at the top of the food chain. Similarly, Congress began to pay more attention to pollutants following passage of the first Clean Air Act in 1963.

By the late 1960s, environmentalists, politicians, community activists, conservationists, scientists, and public health officials understood that lead was one pollutant that challenged them all. It was in the air people breathed and, as the previous decade had made clear, it was on the walls of the nation’s housing. With the new decade, physicians were more effectively treating the symptoms of acute lead poisoning, public health personnel were active in establishing more lead-screening programs to identify children most at risk, and community groups and others were calling for stronger housing codes and more effective enforcement for existing ones. But as they seemed on their way to solving one problem, all through the 1970s they would discover new ones that were in some ways ever more troubling, uncovering literally millions of children at risk of developing life-changing neurological and behavioral problems from the slightest exposure to this devastating metal, while intense resistance from the lead industry continually tried to discredit the new research.

AN INADVERTENT ADVOCATE

Within the government, a federal official played an instrumental role in getting Washington to acknowledge the importance of childhood lead poisoning. Jane Lin-Fu came to her work by a circuitous route. Born in Singapore of Chinese parents, Lin-Fu spent her early years in Shanghai, where her father, a teacher educated in China and the United States, joined his brother Lin Yutang, then a rising journalist, to work as a journalist at China Critic, an English-language periodical. Her father, a Quaker, had a strong sense of social justice, and she still remembers how upset he was by the British treatment of Gandhi. Her mother was well-educated, pragmatic, a strict disciplinarian and a devout Christian. Jane was raised to believe she shouldn’t worry what others thought as long as she was doing the right thing before God. “This upbringing molded me to be the free spirit who would take up social justice issues like lead poisoning, speak the truth about lead as I saw it, and not be intimidated by bureaucratic or academic authorities,” she believes.¹

In 1937, when the Japanese Army invaded China, her parents fled with her to the Philippines, where Jane later attended medical school before coming to the United States in 1955. She accepted an internship, followed by a pediatric residency, at Brooklyn Jewish Hospital, an institution that served many children from the impoverished neighborhoods nearby—in what was later referred to as the “lead belt.” One summer, a two-year-old came to the clinic with a stomachache and vomiting. The physician thought the boy had summer flu but admitted him because he was quite dehydrated. On the ward, the child began convulsing and the attending doctor mentioned it might be lead poisoning. The event made a lasting impression on Lin-Fu.²

In the early 1960s her husband joined NASA and they moved to the Washington, D.C., suburb of Bethesda. She was a board-certified pediatrician, but she wanted a part-time job with the federal government so she could spend time with her children. In November 1963, just after John F. Kennedy’s assassination, she was hired by Alice Chenoweth at the Maternal and Child Health Program in the Children’s Bureau.

When Kennedy became president, the plight of his sister Rosemary led him to make a concerted effort to focus the nation’s attention on the study and treatment of mental retardation. The Children’s Bureau, a beneficiary of the subsequent funds appropriated by Congress for that purpose, helped develop statewide screening programs for phenylketonuria (PKU), a genetic disorder that causes mental retardation. Newborn PKU screening was a particularly exciting area then because, for the first time, severe mental retardation in children who suffered from this genetic disorder could be prevented through large-scale screening, early diagnosis, and dietary treatment.

When a colleague happened to ask Lin-Fu in 1965 what she knew about lead poisoning as a cause of mental retardation, the question triggered a flashback to that little boy who had convulsed from lead encephalopathy in Brooklyn Jewish Hospital a few years earlier. As she looked into the issue she was horrified to realize that her own training had not included lead poisoning, even though research indicated the prevalence of the problem in old, poor neighborhoods like the ones surrounding the hospital where she had done her residency. She was also deeply troubled that the Maternal and Child Health Program in the Children’s Bureau, which was so active in preventing mental retardation caused by the PKU condition, was not doing anything about lead poisoning so common in young children living in dilapidated dwellings. “This is really unfair because poor children have no voice in society,” she recalls thinking at the time. She could not understand how “we could ignore such a simple and readily preventable issue.”³ By December 1965, she had reviewed the existing literature on childhood lead poisoning and written a draft report on the subject that was intended as an internal memo. The Children’s Bureau was so impressed, however, that it sent the draft to outside reviewers, including J. Julian Chisolm, and then published it. That became Lead Poisoning in Children, a widely circulated 1967 government booklet that was instrumental in drawing the attention of Congress and the public to the lead problem.⁴

It also attracted the attention of the lead industry. “When my booklet came out in 1967,” Lin-Fu recalled, “the lead industry wanted to reprint it [with a gloss of their own accompanying it], and they hired Hill & Knowlton to contact me. . . . The industry found my early work useful because it emphasized that the [main] problem was lead paint, not all the other [lead-related] environmental issues [such as lead in gasoline, then the dominant interest of the lead industry]. . . . The lead industry kept sending public relations representatives to me to be my friend. They would call to chat and have lunch with me. They would be friendly and try to keep track of my work.”⁵ While the federal government distributed more than 28,000 copies of Lin-Fu’s pamphlet, this effort, as historian Christian Warren puts it, “paled next to the efforts of the Lead Industries Association which distributed 61,000 copies [of Lin-Fu’s work]. . . as part of its free booklet, ‘Facts about Lead and Pediatrics.’”⁶

Lin-Fu’s publication reflected the prevailing view of the time that lead poisoning was a problem mainly limited to “slums” and poor children, largely ignoring lead in gasoline, which exposed all children, rich and poor, urban, suburban and rural. People in public health and community organizations such as the Young Lords and the Black Panthers helped bring this scourge to public attention.⁷ But even so, many practitioners simply did not recognize lead poisoning because the symptoms were nonspecific except in extreme cases. Others thought lead poisoning “went away” when titanium oxide replaced lead as the major pigment in interior paint in the 1940s.⁸

Arthur Lesser, a well-respected federal public health official who was director of the Maternal and Child Health Program in the Children’s Bureau, said to Lin-Fu one day, apparently exasperated by her insistence about the lead issue, “You did not discover anything. We know lead poisoning was there, but this is a housing problem, not a public health problem. You screen children, diagnose them, treat them and send them home to eat lead paint again. Are you going to fix their houses and remove the lead paint? Obviously not. This is a housing problem—what do you want us to do?”⁹

THE EMERGENCE OF “UNDUE” LEAD ABSORPTION

While Lin-Fu remembers herself as naïve, someone who just tried to do the right thing, ignorant of the bureaucratic and political workings of the White House and Congress, she was in fact a very effective political infighter. Although she did not have a public health background, Lin-Fu saw lead poisoning from the position of a pediatrician and a mother of young children. In contrast to the kind of bureaucratic view Lesser expressed, she did not see why a housing problem causing such serious lead poisoning in children was not also a public health problem. As she put it, “It was a football bounced between housing and public health so it went into no-man’s land.”¹⁰ This kind of tension over which agency should deal with childhood lead poisoning would continue to plague policy makers and advocates alike for decades.

Lin-Fu’s pamphlet and her subsequent work on lead poisoning became the basis for the first statement on the subject by the surgeon general of the Public Health Service, Jesse L. Steinfeld. Lin-Fu remembers, “When we finally finished the draft of the guidelines [in the fall of 1970 for childhood lead-poisoning programs] and sent them downtown [to the Department of Health, Education and Welfare secretary’s office], the surgeon general was on duty that weekend, responsible for signing important papers for the DHEW secretary’s office. He signed the paper and saw the significance of the draft, and it became the [basis for the] surgeon general’s policy statement.”¹¹ In November 1970, Steinfeld announced “guidelines for a nationwide campaign against lead poisoning” because “as many as 400,000 children” were estimated to have blood lead levels above 40 micrograms per deciliter—in 1970, a shocking number of children.¹² At the time, children were considered poisoned if their blood lead levels were over 60 µg/dl. This was the level at which many children, though not all, showed classic acute symptoms of lead poisoning—convulsions, coma, permanent neurological damage, and even death. According to the New York Times, Steinfeld recommended screening programs for “all children under six years of age living in old and poorly maintained houses.”¹³

The surgeon general’s policy statement was important, Lin-Fu recalls, “because a new concept of lead poisoning was contained in the document—that of ‘undue lead absorption,’ which was [seen as] an intermediate problem that preceded clinical symptoms. The document challenged the old concept and definition of lead poisoning—those with overt symptoms of profound neurological damage—and introduced the concept of finding children at the phase of undue lead absorption, defined at blood lead levels of 40 µg/dl and over.”¹⁴

The federal government’s acknowledgment that “undue” lead absorption was a danger to children was an important breakthrough. But it was not achieved without a struggle. The ad hoc committee that drew up the DHEW guidelines for lead poisoning, in case impending legislation became a reality, had included Jane Lin-Fu and other DHEW staff along with outside experts, including Julian Chisolm. “Chisolm opposed me [Lin-Fu] on this, as did the chairman of the committee. . . . He and Chisolm thought that I was being too aggressive and impractical to implement screening and follow-up, as New York City was finding 45 percent of its sampling above 40 micrograms.” The chair challenged Lin-Fu: “How are you going to tell local public health officials that they have a lead problem in half of their kids?” And she answered: “That’s their problem. Our job in the government is to tell them the scientific facts, the truth.”¹⁵ It was Chisolm who had originally written a paper stating that the upper limit of “normal” blood lead should be 40 µg/dl, she pointed out.¹⁶ “When he refused to back up his own statement at the meeting, she recalls, “I knew that DHEW’s committee would not let me say [in the draft guidelines] that the upper level of normal should be 40.”¹⁷

As a compromise, Lin-Fu drafted a statement proposing that in cities with overwhelming lead-poisoning problems priority should be given to children whose blood lead levels were more than 60 µg/dl, followed by those with levels between 40 and 60, and then those with levels less than 40. Children of one to three years should be given priority over those of three to six years, and so forth. At the next meeting, Lin-Fu spread copies of the document around the table and said, “This is what I propose.” Chisolm said, “If we include this statement on priority, then dropping to 40 µg/dl in the statement is OK.” But the chair angrily said it was too radical: “I am leaving the government in three months and I don’t really care what happens with this document. If you insist on the 40 µg criteria, after that statement is released, and when all the letters start coming in to the secretary’s office, you will have to deal with this and answer those letters.” “I will,” Lin-Fu said without hesitation. “Deal,” the chairman said, and the final draft included Lin-Fu’s triage concept of dealing with lead poisoning and dropped the upper limit of what was considered the “normal” blood lead level from 60 to 40 µg/dl, with children having levels above 40 considered at risk from undue lead absorption.¹⁸

While Lin-Fu was fighting within the federal bureaucracy to convey a better understanding of and more action on low-level lead poisoning, a few senators and representatives were also trying to address the emerging lead-poisoning epidemic. Responding to pressure from community organizations in New York, Boston, and around the country and from local public health officials, Congressman William Ryan (D-NY) and Senator Ted Kennedy (D-MA) cosponsored bills in 1969 and 1970 to authorize $30 million in federal grants to combat lead poisoning. The Ryan-Kennedy Bill was passed on December 31, 1970, and signed into law as the Lead-Based Paint Poisoning Prevention Act by President Nixon in mid-January 1971. The act was composed of three parts: the first “empowered HEW [the Department of Health, Education and Welfare] to prohibit the use of ‘lead-based paint’ [paint with more than 1 percent lead pigment] in federally constructed or rehabilitated housing” but left unregulated the private housing stock; the second authorized the Department of Health, Education and Welfare “to make grants to cities establishing lead-abatement programs and . . . to establish screening and treatment programs”; and the third authorized the Department of Housing and Urban Development “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 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 ending with death at the highest end of the scale.” He reminded the audience that between 250,000 and 400,000 American children had blood lead levels in excess of 40 µg/dl and asked “how many of these children have behavior disorders, disturbances of cognitive function, or emotional disorders related to this body burden.” The audience already knew that children living “in the urban American ghetto, and whose blood levels are consistently higher than their middle class counterparts, are known to have an increased prevalence of mental retardation, learning disabilities and behavior disorders.”³⁴ Needleman challenged the scientific community to take the next step, to find out whether or not relatively low-level exposure to lead would produce damage. “If a means could be found to identify older children considered asymptomatic with elevated body burdens of lead, the measurement of their neuropsychologic performance, controlling for other factors known to produce developmental deficits, would allow the investigator to more accurately investigate the effects on their brains of sub-clinical exposure.”³⁵