and adults—from gasoline, paint, canned foods, and other widely available consumer products—was an outstanding public health achievement, which in aggregate lowered the average exposure to lead by orders of magnitude. During the 1960s and 1970s, public health authorities joined with various social movements and thereby were instrumental in shaping these regulatory actions and bringing to the nation’s attention the huge number of childhood poisonings. Through coalitions with social reformers, public health authorities were able to press national, state, and/or local authorities to enact legislation and authorize agencies to achieve reforms. Because of reduced exposure consequent to those reforms, children in the United States today rarely go into convulsions or suffer massive brain damage from lead poisoning, although this is still a major problem in many areas of the developing world. Similarly, because of other regulatory action, Americans rarely suffer from the most acute symptoms of mercury poisoning, arsenic poisoning, or radiation exposure.
Concern over acute lead poisoning has given way to recognition of the subtler but often still devastating problems induced by lead ingestion, problems only vaguely considered a generation or two ago. Indeed, researchers in the past few decades have changed our understanding of the effects that comparatively low levels of lead exposure have on the brain of the developing child, and with that our understanding of the potential low-dose dangers of other toxins. Mercury, chromium, and other heavy metals still cause damage to children (and adults) even if exposure is rarely fatal; the level of arsenic in some of our water supply is with good reason a cause of concern to the U.S. Environmental Protection Agency and state health officials.
Low-dose effects of such toxins are not new problems; they occurred in the acute age as well. But they typically went unrecognized as toxic because of the glaring damage that accompanied acute poisonings and the limited technological tools available for identifying very low levels of exposure. Today, though, we need only read the newspaper headlines to see the growing alarm over the potential harmful health effects of, for example, bisphenol A, a chemical additive that mimics estrogen and other human hormones and that is found in a myriad of children’s toys, baby bottles, plastic containers, adhesives, computer-generated taxi and credit card receipts, and a host of other consumer products.23 Or we may point to the emerging controversies over the use of nanoparticles in skin creams and cosmetics, or the chemicals used in flame retardants in children’s clothing and other consumer items. In these and many other instances, it will require broad population-based public health actions to prevent damage, not just direct individual treatment to deal with these substances’ effects.
The decline of the various social movements in the 1970s and 1980s had a telling effect on the public health profession, as it was deprived of the power and energy of political and social allies that could influence legislators and bureaucrats in local, state, and federal agencies. Following the election of Ronald Reagan, even federal agencies whose mission coincided with public health activists were under attack and stymied in their attempts to regulate the environment, identify and remedy unhealthy working conditions, and provide services to the poor. New publicly built housing virtually ceased in these years. In the face of this broad assault, largely at the behest of conservative critics of the Great Society programs of the 1960s, public health activism waned.24
A strategy of avoiding confrontation with the political and economic institutions that impede the solutions for public health problems—and indeed may have given rise to them—has led to avoiding confrontation with the structural impediments to improving public health. This is the dilemma of public health today: For generations, many in the public health field have depended on the laboratory, on the development of the next magic bullet, on new technologies and diagnostic and therapeutic interventions to deal with public health problems. But, like lead, other ubiquitous environmental poisons now raise fundamental problems that cannot easily be addressed by these methods. If detection of endocrine disruption is truly a new frontier in the understanding of reproductive problems or other biological changes, for example, a medical intervention may not be adequate; and even were it possible, dealing with the consequences individual by individual would overwhelm any health system.
If public health professionals are to effectively address the problems of chronic conditions, subtle neurological damage, obesity, and childhood developmental anomalies, they will be forced to confront huge industries that profit from, for example, the production of fast foods, high-calorie drinks, and tobacco. These health difficulties are not simply an issue for public health professionals; they are of course an issue for society as a whole. Public health individuals and institutions can press, but ultimately their success depends on political and economic forces larger than themselves. From the guarantee of an adequate water supply and sewer system to the passage of Medicare and Medicaid, successful public health reforms of the past have depended on social movements and legislative and/or executive action, and the same is likely to be true for effective action on a broad array of toxins, lead included.
THE SCIENCE AND POLITICS OF LOW DOSES
As the character of the lead-poisoning epidemic has changed over the past half century, especially with the elimination of lead from the manufacture of paint and from gasoline, and as the harm to children of nonfatal doses of lead has become more apparent, the focus of research has shifted to the effects of these smaller doses. Results indicate that, though the level of lead exposure may be low compared to what brings on acute episodes of lead poisoning, the effects are far from minor.
Children with even relatively low levels of lead in their blood (even below 5 micrograms per deciliter) have been shown to suffer disproportionately from behavioral problems in school, school failure, hyperactivity, trouble concentrating, difficulty with impulse control, lowered intelligence scores on standardized tests, higher rates of juvenile delinquency and arrests, and ultimately unemployment and failures in life. Further, children with lead exposure are more likely as adults to have physical problems like kidney and heart disorders. The scientific community and many political leaders now recognize that lead poisoning has been among the most important epidemics affecting children in the United States in the last century.
A particular tragedy of low-level lead poisoning is that its “symptoms” are easily confused with myriad other insults suffered by children who grow up in poor communities, whose housing is substandard and whose lives are shaped by poor education, social marginalization, and, in some instances, racism. In a 1990 article Herbert Needleman noted a stunning statistic that brings this issue home: more than half of all “poor black children have elevated blood lead levels,” estimated at the time as exceeding 25 μg/dl.25
Consider, for example, Sam T., the youngest of his family’s nine children, born in June 1990, just as the Kennedy Krieger Institute study was beginning in Baltimore.26 The family lived in an apartment located in one of Milwaukee’s poorest and most lead-polluted neighborhoods, but according to his medical record, Sam “thrived as a baby” and was developmentally normal at the ages at which he started to crawl, walk, and babble.27 Like many lead-poisoned children, his problems began as a toddler, when he began to move more freely around the apartment, mouthing or sucking his fingers after touching the walls, windowsills, or other objects covered with lead paint or dust.28 When Sam was fourteen months old, a routine check found his blood lead level to be 18 μg/dl, at that time almost twice the Centers for Disease Control’s acceptable exposure limit, which had been reduced from 25 to 10 μg/dl in 1991. A few months later, his blood lead level had almost doubled, to 40 μg/dl, and it did not fall below 25 μg/dl at any time tested over the next two and a half years.29 The family moved to a house nearby in an attempt to escape such a heavily leaded environment, but conditions there were no better. In the summer of 1993, when Sam turned three, his lead levels jumped significantly and he was hospitalized for five days while he received chelation treatments, the in-hospital chemotherapeutic blood treatment aimed at leaching lead from the body.30 But by then it was too late to forestall damage.
When Sam entered kindergarten, teachers immediately noticed that he had problems. Within weeks, he was referred for speech and language therapy and was soon, according to the court record,
