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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

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