Bulletin of the History of Medicine

The Unbearable Heaviness of Lead

Ellen Silbergeld

Peter English. Old Paint: A Medical History of Childhood Lead-Paint Poisoning in the United States to 1980. New Brunswick, N.J.: Rutgers University Press, 2001. xv + 254 pp. Ill. $69.00 (0-8115-2987-5).

Why was this book written? Like Brush with Death, by Christian Warren (reviewed in Bull. Hist. Med., 2001, 75: 823-25), Old Paint treats the history of childhood lead-paint poisoning over the past hundred years. Peter English, like Warren, draws upon access he obtained as an expert in litigation (both authors acknowledge this engagement): English was retained by the lead industry, while Warren served as an expert on behalf of several cities seeking compensation from industry. (The reader of this review should be warned that I am cited by both authors and have also participated in this legal contest, as an expert for New York City and Baltimore in lawsuits against the lead industry.) In actuality, Old Paint represents only the latest phase in the struggle for control over the story of childhood lead-paint poisoning. For most of the last century, the lead industry was particularly alert to the importance of this strategy. A highly integrated industry in the United States, the lead producers early in the twentieth century organized themselves explicitly to defend their products against the growing scientific and popular concerns over this toxic metal. Long before Big Tobacco, the lead industry understood the inestimable value of purchasing "good science." To that end the Lead Industries Association, as well as precursor and subsequent lead industry organizations, made substantial and continuing investments in research and researchers to ensure its hegemony over medical opinion. Thus books [End Page 164] like Old Paint and Brush with Death are outside the tradition embodied in histories of industries and industrialists, as noted by Erica Schoenberger. ¹

We can expect an increased production of books like these as a consequence of the rise of toxic tort litigation. This relatively new case law has developed from the opening of legal remedies in the context of environmental risks, circumventing the legal limits still imposed on workers seeking redress of damages due to chemical exposures. Suits by communities exposed to hazardous waste have been recorded most eloquently in print and film in Jonathan Herr's A Civil Action. Suits over lead poisoning began about the same time, in the 1980s, as individual causes of action by children and their guardians against the owners of property where children were poisoned by lead paint. However, the costs of lead-paint poisoning have fallen more heavily upon those cities, like Baltimore, that have attempted to respond to the crisis of health and housing. Since those most at risk for lead-paint poisoning are the urban poor, the costs are directly borne by public health and housing agencies. Lead-damaged children impose additional costs on society, in terms of special education needs, unemployment, and increased risks of criminal behavior, as documented by Rick Nevin and others. ² For that reason, among others, cities like Boston, New Orleans, New York, Providence, and Baltimore in the 1990s brought legal actions against the lead industry to recover these costs. For a variety of legal issues relating to class certification and market share arguments, these suits have met with limited success in the courts.

Historians are now taking the struggle to a broader audience; in addition to Warren and English, David Rosner and Gerald Markowitz have also recently weighed in with a history of the lead industry in the twentieth century. ³ For the historian of medicine and science, it may appear that the discovery process in toxic tort litigation will open up new sources of primary data. However, the ground rules and motivations of legal discovery introduce distortions into the field of inquiry that must be recognized and distinguished from the properly omnivorous nature of historical research in its quest for definitive rather than selective narratives. It would be useful to the rest of us for all of these historians to [End Page 165] reflect upon the impact of their roles as opposing experts in terms of their professional work as historians.

Old Paint raises concerns about the process of turning expert testimony in litigation into historical narrative and analysis. Toxic tort litigation, to prevail, requires a demonstration of knowing. Thus in these large lead cases, the primary question of fact has turned on what did the industry know, and when did they know it? English, not surprisingly, presents very different answers to these two questions, as compared to Warren. Through careful selection of the historical evidence that supports the industry side, English skates over some rather thin ice in his attempts to avoid those landmarks in the scientific literature that challenge his view of the "what" and "when" of knowing. It may be claimed that his employment did not influence his opinions; rather, that industry sought him out because of his preexisting opinions on the origins and progress of knowledge about lead-paint poisoning. Clearly, his text tracks closely the industry's legal position that (a) no one knew much about lead-paint poisoning in children prior to 1950; (b) the lead industry was responsive to early concerns about its products; and (c) the epidemic of urban lead poisoning in children is due to social and other forces entirely separate from the intrinsic hazards of lead-based paint.

Thus, English argues that it is the blighting of inner cities that caused lead poisoning, as formerly well-kept owner-occupied homes fell into decay, as whites fled to the suburbs and African Americans moved into an increasingly dilapidated urban housing stock (p. 103). The indictment of major socioeconomic changes in American society is quite an ambitious turn on the traditional "blame the victim" defense, despite English's attempts to avoid this charge. In my experience, the lead industry and its "experts"—such as Claire Ernhart, a child psychologist who made an extensive career as an expert defending landlords against tort litigation brought by families—were in the past more modest in blaming mothers and children themselves for causing lead poisoning: mothers for their neglectful or ignorant childrearing practices, and children for being stupid a priori and thus prone to eat lead paint. These defenses avoid the obvious: only lead—not inadequate mothers, stupid children, or blighted cities—can cause lead poisoning. It is like claiming, as some used to say and some still do, that immoral behavior causes epidemic diseases, such as the Black Death (Savonarola), or (more modern) HIV and AIDS. Social and behavioral conditions can propagate disease, but they are risk factors only when the agent of disease is present in the population or the environment. English treads closely to the infamous characterization of lead-poisoned children in Baltimore as "little rodents" (see below), when [End Page 166] he claims that another cause of urban lead poisoning was the racial predilection for pica among African American children (p. 111). Pica is not limited to African Americans, ⁴ and is generally thought to relate to trace-element deficiencies.

English makes much of the lack of public policy on lead paint as a source of childhood lead poisoning, prior to its "transformation" into low-level lead poisoning in the 1980s, as evidence for lack of knowledge. This apparent inertia, also described by Warren, was due to many factors. Of importance was the lack of legal or institutional power to prevent or limit the use of lead in paint, prior to the major governmental reforms of the early 1970s that resulted in the creation of the EPA, OSHA, and the CPSC, so that no action could be taken at the federal level; in 1925, for example, when the federal government reviewed the addition of tetraethyl lead to gasoline, a special commission had to be convened by the Bureau of Mines and the Public Health Service. Second, there were attempts by state and local authorities to prevent uses of lead in housing, but owing to the lack of statutory authority, the industry was able to override these initiatives. Third, starting in the early 1970s there was a highly calculated campaign by the Department of Housing and Urban Development, led by Irwin Billick, to frustrate the implementation of the Lead Based Paint Poisoning Prevention Act, by diverting attention to lead in gasoline and away from lead in housing. This strategy succeeded so well that federally funded actions on lead in housing did not pick up speed until after the war on lead in gasoline was over. Julian Chisolm warned me, in the late 1970s, not to forget the children and their houses, as I began to work on eliminating lead from gasoline.

However, rather than recite the disagreements among these recent books in detail, I choose to consider their agreements on the process of "knowing" lead poisoning. English and Warren, in particular, argue that lead poisoning is best understood as a social phenomenon rather than a scientific or medical entity. It is true that diseases are in many ways socially constructed. They are often named after the practitioner who took the step of calling by one name a set of observations (signs and symptoms, very semiotic) hitherto undefined as a distinguishable entity—hence, Parkinsonism, Alzheimer's dementia, Huntington's chorea, Chagas's disease. Once proposed, the nosology of disease is subject to both centrifugal and centripetal forces; formerly distinct diseases are [End Page 167] lumped together, and formerly unitary nosologies fall apart, with advances in knowledge that can be traced in the great book of names, the Manual for the International Classification of Disease. However, it is a very different matter to assert that because diseases are named, they are therefore entirely social inventions. This view is not new: following the great explosion in the nosology of neuropsychiatric diseases, some physicians and philosophers (R. D. Laing, Michel Foucault, Thomas Szasz) counterattacked, charging that these diseases were deliberately created as instruments of social control. A similar attack on the physical reality of disease comes now from those who prefer to define disease and therapy in spiritual and psychic terms, such as Deepak Chopra and Andrew Weil, following in the pioneering footsteps of Mary Baker Eddy.

So is lead poisoning a construct, and for whose benefit (and by whom) was it constructed? English agrees that there is a "real" lead poisoning, the high-dose acute intoxication described in workers for more than three hundred years prior to the "invention" of childhood lead-paint poisoning in (or about) 1902 (this disputed date figures large in the question of "when"). Industry even admitted this as well, after investigations into the devastating diseases among workers in the lead trades, in the nineteenth century; however, the industry response included an attempt to divide lead into "good" and "bad" compounds (an argument that served the interests of promoting tetraethyl lead as a "gift of God," to use Standard Oil's felicitous phrase at the 1925 hearings, rather than the scourge of public health that it was recognized to be fifty long years and tons of lead later).

But the "what" of childhood lead-paint poisoning has two aspects under intense dispute in litigation: the poisoning of children, specifically, and the poisoning of children by lead, specifically. English does not clearly distinguish between these issues; his increasingly annoying little puzzle diagrams especially fail to make this point. The historical record is quite clear that for nearly 150 years children have been recognized as victims of lead through their employment alongside adults in trades where lead was present (such as mining and smelting, glazing and porcelain production, fabrication of lead bottle-caps). "Fouling the nest" (to use Julian Chisolm's vivid simile)—the special dangers of perioccupational exposures to lead—was also recognized as a hazard for children, including fetuses, as their mothers were employed in the lead works and as pollution from lead industries contaminated surrounding communities. English mentions Sir Thomas Oliver, a great figure in public health who has been unfairly neglected for his prescient recognition of the environmental impacts of dangerous industries. However, he does not discuss [End Page 168] Oliver's characterization of lead as a "race poison," by which he meant to emphasize its adverse effects on succeeding generations. ⁵

The inherent dangers of lead paint were also recognized in the nineteenth century, when the term "painter's wrist" was coined to describe the peripheral neuropathy associated with chronic exposures to lead. In fact, an important impetus for the rise of workers' compensation legislation was the recognition of the hazards of lead paint. Among the first actions of the new International Labor Organization, after World War I, was a convention to ban white lead as a base for paint—a convention never signed by the United States, because of our refusal to ratify the League of Nations treaty.

A place and date are often given—Australia, 1902—for the "birth" of the term "disease of habitation" to describe childhood lead-paint poisoning. But is it credible that James Lockhart Gibson was the first to connect the dots, already drawn, between children and lead, and the dots between lead paint and adult disease? Probably not. Lockhart Gibson was the first to deduce that lead was an etiology for an outbreak of neurological symptoms in children in Queensland, Australia, which is quite a different matter. ⁶ Why would he have even considered such an etiology if the premises had not already been established? Recall that this inference was made long before the instrumentation was available to diagnose lead by its presence in blood or urine.

The impact of Lockhart Gibson's prescient differential diagnosis was remarkably rapid. Especially in the United States, pediatricians began to consider lead as a cause of idiopathic "neuritis" in children, and where they looked they quickly found examples of the disease of habitation. Within twenty-five years after Lockhart Gibson's article, Charles Ruddock wrote in JAMA that "a child lives in a lead world." ⁷ From these events, whose impact English disputes, the modern concept of childhood lead poisoning indisputably developed. While arguing about the time course, English and Warren both consider that this development was largely constructed—that is, lead poisoning has not actually increased in prevalence over the past century, but rather the definition of what it means to [End Page 169] be lead-poisoned has changed such that more and more children meet the medical definition of disease. The two authors differ only somewhat in their interpretations of the motives behind this transformation of the meaning of lead poisoning: both argue that it was a result more of changes in public policy due to social activism, than of advances in scientific knowledge.

However, two events in the history of lead-poisoning research challenge this interpretation. First, two of the most important studies on children and lead were conducted serendipitously—that is, not by design, and not in the context of heated social debates. In the early 1970s, Brigitte de la Burdé, of the Medical College of Virginia, was part of a multisite study of neurocognitive and behavioral development among young children enrolled in the first Head Start Programs in Richmond. ⁸ As her cohort grew, it happened that several children were exposed to lead, which was detected only because the study included periodic assessments, including hematologic measurements that provoked de la Burdé to look for lead. Thus she was able to demonstrate for the first time that developmental deficits followed lead exposure, disproving but not eradicating the industry calumny that preexisting stupidity caused lead exposure (a calumny that English propagates in some of his puzzle-grams, and also by his attention to the minor studies of Sigmund Pueschel and others). Some twenty years later, David Fergusson and colleagues in Christchurch, New Zealand, decided to examine lead exposures in a cohort they had enrolled from birth to study "normal" development among healthy and socially advantaged children. Their results were dramatic: no threshold was observed for the negative correlation between tooth lead levels and behavioral and neurocognitive status. ⁹

The second challenge to the purely "social" explanation for modern concepts of childhood lead poisoning is the role of experimental research, as well as epidemiology, in the rapid transformation of the definition of lead poisoning from an acute intoxication that, absent near-fatal encephalopathy, left no harm, to a widespread, chronic condition that impairs neurological development in the absence of detectable symptoms at the time of exposure. The ability to demonstrate both the manifestations and the mechanisms of a human disease in an animal counters the assumption that environmental diseases such as lead poisoning [End Page 170] arise purely out of a social or political context. Studies of children, by Herbert Needleman and others, were remarkably paralleled throughout the 1970s and 1980s by studies of increasingly lower lead exposures in rats and mice. ¹⁰ This research, unconfounded by social agendas or public health politics, has demonstrated the physical reality of low-level lead poisoning. Through this work, we know much about the neurobiological bases of the persistent neurotoxic damage induced by lead in the developing brain: that is, the molecular mechanisms responding to very low concentrations of lead in terms of altered signal transduction and synaptic strengthening, events that are the biological substrates of learning, attention, and memory. Felix Wormser, secretary of the Lead Industries Association, characterized the poor, black, and lead-poisoned children in Baltimore as "little rodents"; ¹¹ in large part, it is the little rodents of science that closed down his industry's smelters in the wake of banning lead from paint and gasoline.

Nonetheless, it is sadly evident that understanding and thereby preventing lead poisoning has been extraordinarily impeded by the successful manipulation of both history and science by industry through its paid corps of eminent scientists at institutions such as Harvard and the University of Cincinnati. Only with the rise of alternative sources of research support, from government agencies such as NIEHS and EPA, did an alternate body of knowledge, and then an alternative history of this knowledge, come into being. It is to be hoped that readers of this book will take warning. If knowledge is power, the balance of power may have finally shifted for lead, asbestos, and tobacco, but similar struggles over the "what" and "when" of environmental and occupational hazards continue to impede preventive health policy and just compensation. This is a book that still needs to be written.

 

Ellen Silbergeld is Professor of Environmental Health Sciences, Bloomberg School of Public Health, Johns Hopkins University, 615 North Wolfe Street, Baltimore, MD 21205 (e-mail: esilberg@jhsph.edu). She received a B.A. degree from Vassar, and a Ph.D. degree from Johns Hopkins. She has conducted toxicological and epidemiological research on lead poisoning for over 25 years, including studies on mechanisms of neurodevelopmental toxicity, exposures of children and adults to lead, and the remobilization of lead from bone at menopause. She has advised state, federal, and international organizations on lead poisoning prevention, including EPA, CDC, WHO, and HUD. Her research on lead has been recognized by the Barsky Award of the American Public Health Association and a "genius" grant from the MacArthur Foundation.

Notes

1. Erica Schoenberger, "Corporate Autobiographies: The Narrative Strategies of Corporate Strategists," J. Econ. Geog., 2001, 1 : 277-98.

2. Rick Nevin, "How Lead Exposure Relates to Temporal Changes in I.Q., Violent Crime, and Unwed Pregnancy," Environ. Res., 2000, 83 : 1-22.

3. Gerald E. Markowitz and David Rosner, Deceit and Denial: The Deadly Politics of Industrial Pollution (Berkeley and Los Angeles: University of California Press, 2002).

4. For example, see Aysha Khan et al., "Low Level Lead Exposure and Blood Lead Levels in Children: A Cross Sectional Survey," Arch. Environ. Health, 2001, 56 (6): 501-5.

5. Thomas Oliver, Lead Poisoning: From the Industrial, Medical, and Social Points of View (New York: Hoeber, 1914).

6. James Lockhart Gibson, "A Plea for Painted Railings and Painted Walls of Rooms as the Source of Lead Poisoning among Queensland Children," Australasian Med. Gaz., 1904, 23 : 149-53.

7. Charles Ruddock, "Lead Poisoning in Children," JAMA, 1924, 82 : 1682-86.

8. Brigitte de la Burdé and M. L. Choate, "Early Asymptomatic Lead Exposure and Development at School Age," J. Pediatr., 1975, 87 : 638-42.

9. David Fergusson et al., "A Longitudinal Study of Dentine Lead Levels, Intelligence, School Performance, and Behavior," J. Child Psychol. Psychiatry, 1988, 29 : 781-824.

10. Deborah Rice and Ellen Silbergeld, "Lead Neurotoxicity: Concordance of Human and Animal Research," in Louis Chang, ed., Toxicology of Metals (Boca Raton, Fla.: CRC Press, 1996), pp. 659-76.

11. Gerald E. Markowitz and David Rosner, "'Cater to the Children': The Role of the Lead Industry in a Public Health Tragedy," Am. J. Public Health, 2000, 90 : 36-46.