By the time these uncertainties were reduced to a level to support a new consensus on lead's hazards in the early s, thousands of tons of lead had been dispersed into the environment. The responsibility for this catastrophic mistake to use the terms of Carl Shy must be shared among industry, government, and academic researchers. Lead poisoning is an entirely preventable disease, induced by exposures to lead.
The toxicity of lead has been recognized for almost as long as this useful metal has been mined, smelted, and used by human societies 34 , 42 , Rules prohibiting the use of lead additives in beverages were among the earliest food regulations in Europe and the American colonies 18 , Although it was recognized as early as the mid-nineteenth century that children might be among the most vulnerable to lead toxicity [for discussion of early opinions and observations, see Reference 50 ], specific attention to children as a population at risk was only formalized in the s.
Hamilton 26 directed attention to the devastations of occupational and peri-occupational exposures for young children; she recommended that young children be excluded from employment in the lead trades, and that measures be taken to reduce the transport of lead dusts from the workplace to the home.
In , the Australian pediatrician Lockhart Gibson reported on cases of young children intoxicated by lead from lead-based paints used on porches and doors The importance of lead paint as a cause of lead toxicity in children was soon reported in the United States, in Baltimore and in Boston [see 54 for a history of the recognition of lead paint poisoning in the United States]. The definition of lead poisoning—that is, at what level of exposure clinical toxicity occurs—has changed markedly over the century. Over this period, medical and public health opinion has shifted dramatically, from assuming that only high-dose, overtly encephalopathic exposures were significant, to the recognition that very low doses, without clear symptom presentation, are associated with measurable neurotoxicity.
Similarly, concepts related to treating lead poisoning have also undergone profound change.
Prior to , it was generally assumed that if the child's exposure was promptly reduced, then the effects of lead were reversible unless severe toxicity had been induced such as coma and convulsions. After the introduction of the chelating agents ethylenediamine tetraacetic acid EDTA , d-penicillamine, and British anti-Lewisite BAL into therapeutic practice in the s and s, drug treatment was added to reduction of exposure as the means of medical management Although there is a large medical literature associating chelation treatment with reductions in blood lead levels and increased excretion of lead in urine, there is much less evidence that treatment actually affects outcome.
Needleman and colleagues 45 demonstrated through a careful prospective study that early lead exposure affected children's behavior and intellectual attainment for at least 10 years. Thus it is not clear how much benefit, in terms of reversing toxicity, any postexposure treatments bring. Chelation is undoubtedly valuable to lower high blood levels of and prevent acute neurotoxic effects, such as convulsions, as well as reducing effects of lead on kidney from prolonged high-dose exposure.
Extended chelation can reduce overall body burdens of lead as well, including lead in bone 51 , Nutrition may play a role in reducing absorption of lead 27 , but there is little evidence that essential elements, such as calcium or iron, can counteract the presence of lead at target sites of action once it has been absorbed.
These findings have had profound impacts upon strategies for prevention. Nevertheless, current public health policies remain imperfect instruments for achieving progress in primary prevention. In large part, this relates to the complexity of source reduction and to continuing controversies over the value of such strategies as universal screening. The prevalence of childhood lead poisoning is largely determined by two factors: age and proximity to environmental sources or media contaminated by lead.
Other factors that have been associated with increased levels of lead in blood—sex, income, race, place of residence—are mostly predictors of exposure.
Children's blood PbB lead levels are generally highest between 9 and 18 months of age see 2 , 8. This is because children in this age range tend to explore their immediate environments intensively, with a good deal of hand-to-mouth activity 11 , 12 , and as compared to adults they are also more efficient, by five- to tenfold, at absorbing lead taken in orally Some children have an abnormal pattern of ingesting non-food items, often soils pica , which, if these soils are contaminated by lead, can result in very high doses of lead.
Boys have slightly higher levels of PbB than girls, which is thought to be behavioral, related to a greater frequency of exploratory behaviors in early childhood. Nutrition and genotype play a very slight role in modifying PbB 27 , The variables of income, race, and residence signify the social tragedy of lead poisoning in the United States.
The poor and disadvantaged are more likely to live in lead-contaminated environments, especially in dilapidated housing with flagrant lead paint hazards; they are more likely to live in urban neighborhoods where years of traffic have left tons of lead deposits from leaded gasoline; they are more likely to live near point sources of lead, such as smelters, or hazardous waste sites The fact that lead poisoning is not evenly or randomly distributed among children in the United States continues to raise tremendous obstacles to its prevention. This assumption was based on very limited data and highly skewed attempts to identify children with elevated blood lead PbB levels.
Concerns for lead poisoning waxed and waned with social concerns for the disadvantaged until the results of the first representative national survey of lead exposures in US children began to be published in Coupled with the newer experimental and clinical studies demonstrating toxicity at lower levels of lead exposure 42 , these national prevalence reports substantially transformed lead poisoning as a public health issue by making it an environmental concern for the general public for instance, Environmental Defense Fund.
In the absence of national legislation or suitable government institutions, attempts to prevent lead poisoning over the first 70 years of this century and earlier were undertaken only by states and cities. Certain uses of lead, such as lead adulterants to cider and wine, were recognized to pose risks of excess exposure, and these were restricted on a local basis in Europe and the American colonies 18 , Other proposals—such as banning lead in plumbing, proposed as early as the eighteenth century in England 32 —were resisted by the lead industry, which in organized itself to fight attempts to restrict its products The Lead Industries Association succeeded for years in stopping many regulations on lead, including blocking the United States from signing the International Labor Organization ILO convention prohibiting use of white lead in paint, an international treaty that the United States has never signed 48 Table 1.
Most attention until focused, with reason, on occupational lead poisoning. As documented by Hamilton 26 , thousands of workers annually were poisoned by lead in industries ranging from ceramics through battery manufacture. She also reported on the poisoning of children through their employment in the lead trades, and through the uncontrolled movement of lead dusts from the workplace to the worker's home, which remains a continuing problem Some children were screened, starting in Baltimore in , with the development of laboratory methods at Johns Hopkins But from to , fewer than children were tested with the dithizone method No actions were taken during this time on lead in environmental media such as air or water, in the absence of any comprehensive environmental legislation.
An attempt was made in the s to reduce allowable residues of lead in food lead arsenate was widely used as a pesticide , but this was defeated by heavy industry lobbying. The production and consumption of lead in the United States continued to grow. Worse, in , a new use of lead was approved, and this was to become the largest single source of lead contamination in history.
The decision to permit the use of alkyl lead additives in automobile fuels represents the greatest single failure in preventing lead poisoning. As shown in Figure 1 , the greatest increase in human use of lead occurred at this point in time note log scale on y-axis. This increase was quickly followed by rises in lead concentrations measured in stable ecological indicators, such as Greenland ice 42 , How the lead, gasoline, and automobile industries convinced the US Public Health Service to approve lead for gasoline has been eloquently described 58 , A sample of the industry propaganda of the time is shown in Figure 2.
Despite the objections of Hamilton and others, a US government commission decided in to permit tetraethyl lead TEL use in gasoline, with a promise to reconsider the issue later This phase of the prevention struggle has been source directed, rather than case oriented. For the first time, dedicated efforts were made to identify and prevent lead exposures prior to exposure of children.
These efforts took two forms: setting enforceable standards for environmental media and drinking water, and specific restrictions on certain uses of lead. These actions are summarized in Table 2 Sometimes these actions flowed together. In a similar fashion, the EPA's decision to reduce the drinking water standard for lead from 50 ppb to 5 ppb, in , resulted in bans on use of lead in plumbing solders and fixtures to avoid exceedances due to leaching of lead into drinking water. These actions to improve environmental standards and to restrict lead uses had major effects on the nature and extent of lead poisoning in US children over the s.
Controls on lead in other products, such as increased vigilance by the FDA and CPSC over imported foods and toys, also probably contributed to these substantial reductions 2 , Use of lead in house paint had been restricted by regulation in , but, for reasons discussed below, this action has had little short- or medium-term impact on lead exposures.
The most dramatic and creative effort at primary prevention was an economic disincentive against lead consumption, introduced as legislation by Congressman Ben Cardin of Maryland in This initiative failed in an anti-tax climate, but it represents something of a high-water mark in public health strategies in primary prevention.
Screening is an important aspect of disease prevention, through the early identification of increased exposures and the prompt delivery of therapeutic interventions. Screening not only identifies individuals at risk, but it can also permit health authorities and others to identify sources of lead and reduce or remove them prior to other children being exposed. Screening for lead poisoning involves the measurement of lead in blood, or an appropriately sensitive and specific biomarker of exposure.
For lead, the biomarker of erythrocyte protoporphyrin EP , a biological precursor in the cellular synthesis of heme, was widely used to diagnose lead exposures. This test was highly successful in facilitating screening because it was relatively cheap and, most importantly, with the hematofluorometer, results could be quickly obtained under clinic or field conditions 10 , Screening increased in the s in many cities and states until the early s, when screening decreased in the face of efforts to defund public health programs and roll lead screening into underfunded block grants to the states.
The only recommended methods for screening involved careful collection of blood by venupuncture and lead analysis at a technically competent laboratory The costs increased and logistics become more complicated. The successful regulation of certain lead sources substantially lowered average PbBs in children in the United States, from to As shown in Figure 3 , the distribution of PbBs has shifted dramatically.
The role of removing lead from gas in this reduction was clear from a trend analysis of the NHANES II data collected from to , a period that coincided with the first major phasedown of lead in gasoline Figure 4. While this change must be considered a public health success, this very success has reduced the momentum to fully eliminate lead poisoning. For these children, lead paint is the overwhelming source of exposures 61 , 73 , followed by exposure to highly contaminated urban soils that contribute to household dusts However, as found by Ashley et al 3 when lead-painted surfaces are present in a home in poor condition, the paint source dominates in house dust and children's blood.
Reviews of Environmental Contamination and Toxicology attempts to provide concise, critical reviews of timely advances, philosophy and significant areas of. Reviews of Environmental Contamination and Toxicology (v. ): Medicine & Health Science Books @ bruneslichaf.tk
Lead-based paint in housing has been the most significant source of high-level lead exposure for most of this century. As shown in Table 4 , it is the most significant source of lead exposures for young children 1. Despite early recognition, restrictions on the use of lead in paint in the United States were successfully thwarted by the concerted actions of the organized lead industry The city of Baltimore, under the inspired leadership of Huntington Williams, banned the use of lead-based paint in public housing, but it was not until that the US Consumer Product Safety Commission finally issued regulations limiting the concentration of lead in paint to 0.
However, the regulations covered only paints on indoor surfaces of residential structures, and articles such as toys and furniture designed for use by children.
More seriously, these steps could not deal with the lead paint that had been used in housing before the ban. As documented by the Department of Housing and Urban Development, over 40 million residential units in the United States are estimated to contain lead-painted surfaces because they were built before Table 4.
Of the 42 million units, some 26 million are in dilapidated condition 73 , such that lead paint hazards are more likely to present risks of exposure through contamination of house dust and presence of paint flakes and chips 14 , Their distribution varies with the age of communities; Massachusetts, Illinois, New York, New Jersey, and Pennsylvania have millions of these units.
Dealing with existing lead paint in housing has proved difficult because of the complex of issues related to poverty, housing, and disease prevention. Housing is an unusual vector of disease: It cannot simply be eradicated without provision of adequate substitutes.
When the most dangerous housing is in poor neighborhoods, the social concerns of providing any affordable housing for the poor can come into conflict with preventing disease. The provision of lead-safe housing has been estimated to require major public or private investments, costing billions of dollars Public policy, where it has existed usually on the local level , has placed the burden on the private sector to abate lead hazards when identified.
For example, by , Baltimore had developed, on paper, the most rigorous legal standards to require landlords to remove all lead paint from homes where children with elevated PbB were found. They evaluated the economic resources for private sector lead-paint abatement in Baltimore and concluded that landlords could not recover the costs of adequate abatement from the revenues that could be generated from rental housing in poor neighborhoods.
They warned that existing laws, if fully enforced, would result in large-scale abandonment of housing and a loss of affordable housing for the poor. Their analysis was quickly taken up by property owners' organizations to attack lead poisoning prevention programs in Baltimore, New York, and elsewhere. Their concerns were shared, for different motivations, by some advocates for housing and community development, such as the Enterprise Foundation.
The controversy was considerably heightened by the success of attorneys for some children and their families in winning large judgments and settlements against property owners. Despite applied research projects demonstrating that adequate hazard reduction could be achieved for substantially lower costs than first estimated 19 , 20 , the conflict remained. It came to a head after , when legislation related to lead-paint poisoning prevention had been passed through the efforts of Senators Alan Cranston of California and Paul Sarbanes of Maryland, among others.
The Housing Act attacked the lead-paint problem in three ways. First, it closed a loophole in occupational health, whereby abatement and construction workers had not been covered by the OSHA lead standard Second, it enlisted market forces to encourage abatement by requiring disclosure of lead paint in private real estate transactions. Third, it required HUD to develop policies for dealing with private and public rental housing, particularly for poor and low-income families. The success of disclosure and notification to prevent lead poisoning in children is unknown.
Some anecdotal evidence suggests that it has worked in Boston in terms of increasing the amount of abatement S Pollock, personal communication. But it has served to separate the lead poisoning problem of the affluent from that of the poor. The poor are more likely to be renters than owners, and their housing is in many cases insufficiently valued to absorb the costs of abatement without public subsidy. The problem of low-income housing was given by HUD to a national task force to resolve.