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      FIGURE 2.Lead (Pb) deposited from leaded gasoline in U.S. cities, 1950-1982. Gasoline was a main source of lead that damaged many, particularly urban, children until the 1980s. The amount of lead in gasoline was gradually reduced from 4 grams per gallon to 0.1 gram per gallon in 1986. It was finally completely phased out of gasoline for automobiles in 1996. Source: Howard W. Mielke, Mark A. S. Laidlaw, and Chris R. Gonzales, “Estimation of Leaded (Pb) Gasoline’s Continuing Material and Health Impacts on 90 US Urbanized Areas,” Environment International 37 (January 2011): 248-57, available at www.sciencedirect.com/science/article/pii/S016041201000156X.

      Patterson’s critique of lead’s ubiquity and its potential danger to the public came at a critical time for the industry. Historically, lead pigment had been the most economically significant market for lead producers, but it had begun declining in importance as latex and titanium pigments increasingly captured market share. As automobile sales mushroomed with the economic boom following World War II, the auto industry and the producers of batteries and leaded gasoline supplanted users of pigments as the major buyers of lead. Between 1940 and 1960, despite less frequent use of lead in interior paints, lead consumption increased from about 600 short tons to approximately 1,000 short tons per year. During this period, lead for use in gasoline increased eightfold, from about 25 short tons to just under 200; and lead used in batteries doubled, from 200 short tons to just under 400. Despite the increasing evidence of lead’s destructive environmental effects, during the 1960s and the 1970s lead production increased substantially. In 1964, the United States consumed 1,202 short tons of lead. By 1974, this had grown by about 25 percent, to 1,550 short tons.⁶⁷

      Patterson was not alone in taking on Kehoe’s paradigm. In 1966 Harriet Hardy, one of the nation’s preeminent occupational health physicians, condemned the lead industry’s threshold idea of harm based on adult lead workers; she argued it was inadequate as a means of protecting high-risk populations outside of the workplace. As coauthor, with Alice Hamilton, of the main textbook in occupational medicine, she argued that certain vulnerable populations—particularly children and pregnant women—might suffer the effects of lead at much lower levels of exposure than male workers did. Hardy also delineated the inadequacies in earlier definitions of lead poisoning, arguing that lead poisoning produced a host of subtle and difficult-to-define symptoms (such as fevers, lethargy, and joint pain), but no less damaging for that, which could easily escape the notice of physicians. “It is necessary to emphasize,” she wrote, “that no harmful effect of lead is unique [to that poison] except perhaps the motor palsy of the most-used muscle group, as in the wrist drop.”⁶⁸

      Hardy believed that the developing child was most at risk. Randolph Byers and Elizabeth Lord’s research in Boston on long-term effects of acute lead poisoning, along with clinical observations by doctors such as L. Emmett Holt, John Ruddock, Charles McKhann, and Edward Vogt, supported Hardy’s opinion that lead was more toxic to the young than to the adult population.⁶⁹ In contrast to Kehoe, who used adult males in his studies and in his model of classic lead poisoning, Hardy recognized that a much wider net had to be cast to understand the full range of lead’s effects: “Prevention of diagnosable Pb poisoning in healthy male workers is important but not enough in our society.” Lead was a known toxin, and there was “no available evidence that lead is useful to the body,” particularly for women and children.⁷⁰

      In the coming years, the policy model that Patterson first proposed—that lead, a known toxin, should not be widely introduced into the human environment, and that Hardy expanded to specifically include women and children—would be embraced by those who pushed for the removal of lead from gasoline, and, hence, from the atmosphere.⁷¹ This was an early statement of what, generalized, would become known as the “precautionary principle”—the basic idea behind public health, that, when considering the use of new or suspect chemicals, it is prudent to prove them safe rather than waiting to see if they are harmful to people or the environment. Hardy quoted Bradford Hill, the eminent English epidemiologist who, with Sir Richard Doll, demonstrated the relationship between cigarette smoking and lung cancer: “All scientific work is incomplete. . . . All scientific work is liable to be upset or modified by advancing knowledge. That does not confer upon us a freedom to ignore the knowledge we already have, or to postpone the action that it appears to demand at a given time.”⁷²

      SOCIAL ACTION AND LEAD POISONING

      Until the mid-1960s, lead poisoning—whether from lead paint, lead in gasoline, or lead in the factory—had remained, beyond the victims themselves, largely an issue for clinicians and researchers in a few major medical centers around the country, a small group of public health professionals, and an industry intent on protecting its market. But this changed as the civil rights movement galvanized the African American community and forced middle-class white Americans to acknowledge the extent of endemic poverty and racism. Michael Harrington’s 1962 book, The Other America, and the civil rights–era sit-ins, Freedom Rides, voter-registration campaigns, and school-desegregation drives all made poverty and racial discrimination headlines in daily newspapers across the country.

      As the War on Poverty took shape in the years following John F. Kennedy’s assassination, the links between poverty, housing, and racism in the nation’s cities became increasingly apparent to many Americans. Lead poisoning—particularly from peeling paint in slum housing—became a signature disease of poverty. In New York City, the number of children identified as lead poisoned, now defined as 60 or more micrograms of lead per deciliter of blood shot up from 20 in 1952 to 509 by 1965; in Philadelphia, from 2 in 1952 to 163 in 1965; in Chicago, from 33 in 1953 to 304 by 1966. This was not because more children were affected but because more public health authorities and doctors were now conscious of lead poisoning’s existence and its array of symptoms.⁷³

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