Lead was shown to be a poison around 2,000 years ago by the Greek physician Pedianos Dioskorides, whose medical manual continued in use for more than 15 centuries. Although in ancient Rome and in some medieval settings lead was widely used, so far scholars of those eras have found little evidence that lead poisoning was recognized as more than an occupational hazard, mostly affecting mine and smelter workers.
The industrial revolution, starting in Europe during the late eighteenth century, brought a surge in the use of lead and a corresponding surge in lead poisoning. In England, a physician found the “Devonshire colic” was lead poisoning in 1767, caused by apples crushed into cider with lead implements. Otherwise, until the late twentieth century, the great majority of lead concerns continued to focus on workplace hazards.
Diagnoses: Frank symptoms of lead poisoning tend to set in at blood concentrations around 40 ug/dl (micrograms per deciliter) or 2 uM (micromolar). They become acute around 80 ug/dl or 4 uM. Before the 1960s, there were no reliable tests to measure such relatively small concentrations, less than a part per million. Testing environments were often lead-contaminated, especially after leaded gasoline began to be sold as motor-vehicle fuel in the 1920s. Test results might differ by factors of four or more. Diagnoses relied heavily on observations rather than on tests and almost always focused on acute symptoms.
Acute lead-poisoning symptoms include skin pallor, constipation, intestinal cramps, muscle spasms or paralysis, hallucinations and a “lead line” visible in the gums. Early tests included “stippling” of erythrocytes in blood, described in 1899, and opaque bands seen in X-rays near the ends of bones, described in 1943. By the time those tests showed problems, though, lead exposures had become profound.
A rare report about chronic effects of lead exposure described children who had apparently recovered from an acute episode of poisoning. Elizabeth Lord, a child psychologist at Boston Children’s Hospital from 1929 to 1942, followed 20 chidren for several years. She and Randolph Byers, a pediatrician at Children’s from 1925 to 1971, reported that all but one of those children showed learning disabilities persisting from infancy into early childhood, when they no longer had acute symptoms.
Automotive threats: The most significant and widespread source of lead for most modern environments in the United States was leaded gasoline, used as motor-vehicle fuel. Its chief sponsor in the 1920s was General Motors–as part of a struggle for market share with Ford and smaller competitors, with promises of “comfort, convenience, power and style” according to G.M. advertising.
In 1922, Charles F. Kettering, vice president for research, and Thomas Midgley, Jr., chief chemist, filed a patent application for tetraethyl lead as a gasoline additive to prevent engine knock and increase power (U.S. Patent 1,492,953 issued in 1926). The main alternative had been grain alcohol. The patent gave G.M. a major advantage: unlike an approach using alcohol, G.M. could control the market and reap monopoly profits.
Led by Kettering, General Motors entered into partnership with DuPont to produce trtraethyl lead and began a campaign of promoting so-called “Ethyl” gasoline and trying to discredit objections and alternatives. From the late 1920s through the early 1970s, nearly all U.S. automobiles and light trucks used leaded gasoline. Over about 80 years, more than seven million tons of lead entered U.S. environments from motor vehicles.
Measurements: In 1964. Sir Alan Moncrieff and others at Children’s Hospital in London tried to extend the Byers and Lord investigations, measuring blood lead in about 200 children. They used an optical absorbance technique, reporting substantial variations for repeat measurements. They found nearly all children evaluated as psychologically normal had blood lead under 40 ug/dl and those evaluated as retarded or disturbed had levels up to 70 ug/dl. They did not follow subjects over extended times.
In 1971, researchers at the Connecticut School of Medicine described a method using a then new technology of atomic absorption spectroscopy to improve sensitivity. They reported a coefficient of variation of 2.7 percent. A small cohort of children regarded as normal all had blood lead under 30 ug/dl. A larger cohort from a depressed area of Hartford had levels up to 150 ug/dl. The researchers did not follow subjects over extended times.
By 1979, a method using atomic absorption spectroscopy reproduced measurements of blood lead with a standard deviation of 2.3 ug/dl, reliable enough to support the CDC “level of concern” of 30 ug/dl (1.5 uM) at the time, although not reliable enough to apply much lower standards to individuals in medical settings. Technologies to measure lead in blood and tissues continued to improve, supporting medical diagnoses as well as stimulating research.
Harmful effects without acute poisoning: Concerns about harms from lead levels lower than those found with acute poisoning were confirmed in the late 1970s. Research organized by the late Herbert L. Needleman, a pediatrician and child psychiatrist at Boston Children’s Hospital, was reported in 1979. It focused on children whose lead exposures had been regarded as normal, using standards from the early 1970s.
Needleman saw signs of lasting harm to children as a young physician working at a community health clinic in Philadelphia. He suspected research would show differences in mental skills and social behaviors that grew with differences in lead exposure. Aware that his research was likely to be closely scrutinized, Needleman and his colleagues assembled a large cohort of subjects drawn from public school populations in Somerville and Chelsea, MA–avoiding, for example, subjects drawn from special schools or from medical clinics.
Because mental skills and social behaviors develop with many influences, Needleman and colleagues compiled background information about each subject that would make it possible to adjust results for a range of social and economic factors. Instead of relying on isolated measurements of blood lead that might not represent exposure history, they took measures of cumulative lead exposure from deciduous “baby” teeth that subjects had shed and provided.
After adjustment for social and economic factors, results in 1979 from Needleman and colleagues showed that as children’s lead exposures increased mental skills decreased and social behaviors became less adaptive. The researchers argued that prevailing standards for lead exposure were far too lax. Based mainly on acute poisoning, those standards ignored lead exposures that would harm children.
Lead from the air: Lead from gasoline, spread through the air, was the most serious and pervasive lead hazard in the United States between about 1930 and 1990. Although researchers and physicians had continued to sound alarms, lead was finally removed from U.S. motor-vehicle gasoline as a byproduct of other environmental concerns, not because of the alarms over lead poisonings and impairments.
In 1954 Arie J. Haagen-Smit, a Caltech chemistry professor, showed that clouds of smog, blighting the Los Angeles area for many years, were mostly produced by sunlight-stimulated reactions of hydrocarbon fumes from motor vehicles. Less frequent but occasionally severe smog attacks were becoming common in other locations. including mountain areas around Denver, CO. Public pressure grew to address the problems.
The Clean Air Act Amendments of 1970 (P.L. 88-206), a legacy from former Sen. Edmund S. Muskie (D, ME), required major reductions in motor-vehicle emissions by 1975. Research during the 1960s had shown that catalytic converters, made with ultrathin layers of precious metals, could achieve the results by oxidizing hydrocarbons in exhaust fumes. However, lead from gasoline would quickly foul those devices.
In 1970, General Motors began a campaign to remove lead from U.S. gasoline, a great irony. Decades earlier G.M. had promoted leaded gasoline, but by 1970 the company had sold its interests in tetraethyl lead and had filed patent applications for catalytic converters. In 1973, the U.S. Environmental Protection Agency issued regulations reducing, in stages, amounts of leaded gasoline allowed to be distributed in the U.S..
Removing lead from gasoline produced prompt declines in surveys of blood lead. By the middle 1970s, blood lead measurements had become fairly reliable, leading the U.S. Centers for Disease Control to add blood-lead testing in a second National Health and Nutrition Examination Survey (NHANES) for 1976-1980–by luck coinciding with impacts of EPA regulations reducing lead in gasoline–as well as in subsequent surveys.
Lowering total lead in U.S. gasoline from about 200,000 tons per year to about 100,000 tons per year (50 percent) paralleled a reduction in average blood lead measured for HNANES II subjects of all ages from about 16 ug/dl to about 10 ug/dl (40 percent). At the peak of production around 1970, leaded gasoline probably caused more than half the total blood-lead burden carried by U.S. residents.
Regulation: As authorized under the Clean Air Act Amendments of 1970, in 1974 the U.S. began requiring new cars to run on unleaded gasoline and requiring retail outlets to make unleaded gasoline available. After 1995, retail sale of leaded gasoline was banned. The long “phase-out” of lead in U.S. gasoline paralleled declines in measurements of blood lead, as recorded by national health surveys.
By 1989, unleaded gasoline accounted for 90 percent of motor-vehicle gasoline sold in the U.S. A statistical analysis performed that year, adjusting for several social and economic factors, found that the reduction of lead in gasoline had lowered average blood lead for U.S. residents by about half.
After gasoline lead, the next most common household lead hazards in the United States have long been paint containing lead pigments, lead in water pipes and fixtures, and lead in soils and dust. These threats are geographically concentrated, as compared with lead from gasoline. They occur mainly in older neighborhoods where leaded paint and lead water pipes were common, near current and former incinerators and coal-fired power-plants, and near current and former industries working with lead.
Before the 1970s, lead pigments were typical major components of paints. The federal Lead-based Paint Poisoning Prevention Act of 1971 (P.L. 91-695) and amendments in 1973 banned most retail sales of leaded paint after 1974. A series of federal laws and regulations starting that year, plus state regulations, gradually restricted uses of lead in water pipes and fixtures. The major federal laws were the following:
— Safe Drinking Water Act of 1974 (P.L. 93-523)
— Safe Drinking Water Act Amendments of 1986 (P.L. 99-339)
— Safe Drinking Water Act Amendments of 1996 (P.L. 104-182)
— Reduction of Lead in Drinking Water Act of 2011 (P.L. 111-380)
Effects on child development: Pursuing Needleman’s work into unexplored territory, in 2005 Bruce P. Lanphear and colleagues at Cincinnati Children’s Hospital and other institutions published data analysis for childhood harm from lead exposure–based on research by other groups. Results indicated major, lasting harm at blood levels below 10 ug/dl (0.5 uM). Lanphear and colleagues estimated IQ loss of about four points for blood lead increasing from 2-1/2 to 10 ug/dl.
Those results drew objections–particularly lack of adjustment for social and economic factors–but they provoked anxiety. The CDC “level of concern” for children’s blood lead had been lowered from 30 ug/dl in 1979 to 10 ug/dl. Echoing Needleman and colleagues from 1979, Lanphear and colleagues argued in 2005 that prevailing standards for lead exposure were still too lax.
In 2008 Todd A. Jusko at the University of Washington and colleagues at several other institutions published a new study of about 200 school children in Rochester, NY, who had been followed for six years. Results adjusted for social and economic factors showed IQ loss of about five points for children with blood lead about 5 to 10 ug/dl, compared with children with blood lead about 2 to 5 ug/dl. Findings from Lanphear and colleagues in 2005 showing harmfui effects of blood lead below 10 ug/dl were thus confirmed.
One might have thought the Obama administration would step into the situation by funding research with much larger subject groups and conducting exhaustive reviews of standards. However, there was no new large-scale research, and it took 3-1/2 years for significant progress revising standards. In May, 2012, the Centers for Disease Control lowered a threshold for blood lead in young children to 5 ug/dl, renaming that a “reference level” instead of a “level of concern.”
As reported by the Boston Globe, in the final days of the Obama administration the EPA “sidestepped the issue of a specific new threshold for acceptable lead levels” of soils in urban environments. The agency provided only “general guidance.”
– Craig Bolon, Brookline, MA, February 26, 2018
Shelia Kaplan, EPA sidestepped decision to tighten standards for lead levels, leaving communities adrift, Boston Globe Media (Stat), March 28, 2017
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Mathy Stanislaus, Memorandum re updated scientific considerations for lead in soil cleanups, U.S. Environmental Protection Agency, December 22, 2016
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Blood lead levels in U.S. children, 1997-2015, U.S. Centers for Disease Control and Prevention, 2016
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See Fig. 2.5, Change in blood-lead levels in relation to a decline in use of leaded gasoline
Herbert L. Needleman and David Bellinger, The health effects of low-level exposure to lead, Annual Review of Public Health 12:111-140, 1991
Michael Weisskopf, Auto pollution debate has a ring of the past, Washington Post, March 28, 1990
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