Subcommittee on Housing and Transportation

Hearing on "Lead-Based Paint Poisoning: State and Local Responses"


Prepared Statement of Dr. Bruce Lanphear
Environmental Protection Specialist
Colorado Department of Public Health and Environment

2:30 p.m., Tuesday, November 13, 2001 - Dirksen 538

Statement of Representation:

I am an employee of Children’s Hospital Medical Center of Cincinnati, Cincinnati, Ohio. I am acting on behalf of the children of the United States.

A Rationale and Strategy for the Primary Prevention of Subclinical Lead Toxicity

Subclinical lead toxicity, defined as a blood lead level of 10 m g/dL or higher, was estimated to affect 1 in every 20 children in the United States (1). The preponderance of experimental and human studies demonstrate serious deleterious and irreversible effects of low-level lead exposure on brain function, such as lowered intelligence and diminished school performance, especially from exposures that occur in early life (2). Collectively, the results of these studies argue that efforts to prevent neurocognitive impairment associated with lead exposure should emphasize primary prevention – the elimination of residential lead hazards before a child is unduly exposed. This contrasts, paradoxically, with current practices and policies that rely almost exclusively on secondary prevention efforts – attempts to reduce a child’s exposure to residential lead hazards only after a child has been unduly exposed. Despite an abundance of recommendations about how to prevent children’s exposure to residential lead hazards, there is a paucity of data demonstrating the safety or benefits of these recommended controls for children with blood lead levels below 25 m g/dL (3).

Although the mechanisms by which lead causes its toxic effects remain unknown, substantial progress has been made in reducing widespread lead exposure. During thepast two decades, average blood lead levels in U.S. children have fallen by over 90%, due largely to the elimination of lead from gasoline, dietary sources (i.e., lead-soldered canned foods and beverages), and residential lead-based paint (3, 5). It is estimated that 890,000 (4.4%) preschool children in the U.S. have a blood lead of 10 m g/dL or higher (1). But in some cities, especially in the Northeastern and Midwestern United States, over 35% of preschool children have blood lead levels exceeding 10 m g/dL from exposure to residential lead hazards (6).

Prior to 1970, lead poisoning was defined by blood lead greater than 60 m g/dL, a level often associated with acute symptomatic disease – including abdominal colic, frank anemia, encephalopathy or death. Since then, the threshold for defining elevated blood lead levels has gradually been reduced. In 1991, CDC reduced the threshold even further, to 10 m g/dL (4). These ongoing reductions in the acceptable levels of children's blood lead were the result of evidence indicating that blood lead levels as low as 10 m g/dL were associated with adverse effects in children, such as lowered intelligence, hearing deficits and growth retardation (2).

Although blood lead concentrations below 10 m g/dL are often considered typical or "normal" for children, contemporary levels of childhood lead exposure remain exceedingly high compared with that of pre-industrial humans (7). Indeed, there is increasing evidence that lead-associated cognitive deficits occur at blood lead lower than 5 m g/dL (8). Collectively, the results of existing research argue for a reduction in blood lead levels that are considered "acceptable" – from 10 m g/dL to 5 m g/dL or lower. They also argue for a shift toward the primary prevention of childhood lead exposure, which contrasts sharply with current efforts that rely almost exclusively on case management of children with elevated blood lead levels (3).

From Screening Children to Housing

Universal screening of children for elevated blood lead levels in the United States is controversial. Elevations in children’s blood lead level are unevenly distributed in the U.S. population - varying by child’s age, poverty level, race, and condition and age of housing (1, 6). Due to the focal distribution of lead exposure, few children are identified as having an elevated blood lead level in some communities. Thus, some pediatricians and public health officials are hesitant or vigorously oppose universal screening. There is no question, however, that because lead exposure is cumulative and its detrimental effects irreversible (9), any strategy that is limited to screening children after an exposure has occurred is flawed (3).

Thus, there continues to be a need to refine screening strategies to target and identify children with undue lead exposure (10). But it is more critical to develop a strategy and expand our efforts to identify and eliminate residential lead hazards before children are unduly exposed.

Residential Sources of Lead Exposure

Paint is the major source of childhood lead poisoning in the United States. Children with blood lead above 55 m g/dL are more likely to have paint chips observable on abdominal radiographs and the majority of preschool children with blood lead over 25 m g/dL are reported to put paint chips in their mouths (11). In contrast, house dust contaminated with lead from deteriorated paint and soil is the primary source of lead ingestion for children with blood lead between 10 m g/dL and 25 m g/dL (12). Over 95% of U.S. children who have elevations in blood lead fall within this range (1).

Residential Standards: Key to Prevention

Under section 403 of Title X, the U.S. Congress mandated the Environmental Protection Agency (EPA) to promulgate health-based lead standards and post-abatement clearance testing for house dust and residential soil. Standards are necessary for screening high-risk housing to identify lead hazards prior to occupancy and before a child is unduly exposed. Residential standards are also critical to identify and eliminate lead hazards for children who already have elevated blood lead levels; major sources of lead will be neglected if dust and soil testing are not routinely done. Finally, standards serve as a benchmark to compare the effectiveness and duration of various lead hazard controls. But if standards remain voluntary, they will not be used nor will they protect children from undue lead exposure.

EPA defines their level of statutory concern as between 1% to 5% probability of a child having a blood lead level in excess of 10 m g/dL. Scientists have estimated, from epidemiologic data, that 5% of children will have a blood lead level > 10 m g/dL at a floor lead level of 5 m g/ft2 - a value almost 10-times lower than the proposed EPA floor standard (13). At a floor standard of 50 m g/ft2, 20% of children are estimated to have a blood lead level > 10 m g/dL (13). Children who are exposed to floor dust lead levels > 25 m g/ft2 are at 8-times higher risk of having blood lead levels > 10 m g/dL compared with those exposed to levels below 2.5 m g/ft2 (13). Thus, the floor standard promulgated by EPA is inconsistent with their definition of blood lead levels that "pose a threat" and does not adequately protect children.

Hazards of Lead Hazard Controls

Lead poisoning is often regarded as a preventable disease. In practice, however, the safety and benefits of measures intended to control or reduce residential lead hazards are uncertain. Interventions to prevent or control childhood lead exposure (called lead hazard controls) have far too often been shown to result in an increase in children’s blood lead levels (14). There is some evidence that lead hazard controls, including paint de-leading or abatement and stabilization of painted surfaces, can reduce lead exposure for children who have blood lead levels > 30 m g/dL (15). In contrast, it is uncertain if lead hazard controls are safe or beneficial for children who have lower blood lead levels. Indeed, paint abatement has been shown to cause a rise in children’s blood lead levels (16). Presumably, this rise in blood lead levels is due to lead contamination from removal or scraping of leaded paint (17). It is likely that lead hazards caused by lead hazard controls or renovation can be eliminated by promulgating effective health-based dust standards and requiring that clearance tests are conducted after any renovation or abatement is complete. But clearance tests or residential lead standards must be empirically derived and protect children from undue lead exposure, as measured by blood lead levels.

The costs to prevent childhood lead poisoning from residential hazards are substantial. It has been estimated, for example, that the first-year cost to reduce residential lead hazards in federally owned or federally assisted housing is $458 million. HUD has estimated the overall benefit, defined as increase in lifetime earnings of children who are protected from the detrimental effects of lead exposure, was $1.538 billion - a net benefit of $1.08 billion (18). This estimate does not, however, include recent findings indicating that the drop in IQ is greater for each 1 m g/dL increase in blood lead at levels below 10 m g/dL (19). Nor does it include other anticipated benefits, such as reductions in cardiovascular disease, tooth decay and delinquent behaviors (20).

Other Residential Hazards

Lead poisoning in childhood is only one of several indicators of our failure to protect children from residential hazards. Children’s health is a function of their home environment. If residential hazards were eliminated, morbidity and mortality among children in the United States would decline dramatically. Moreover, many of the racial and socioeconomic disparities in children’s health would be reduced.

Injuries’, including falls, ingestion and burn injuries, are the major causes of morbidity and mortality in children. Over 50% of fatal and non-fatal injuries in childhood occur in children’s homes (21). Environmental tobacco smoke competes with injuries as the leading cause of disease in U.S. children (22). Over 43% of U.S. children are exposed to environmental tobacco smoke in their homes, leading to a dramatic excess of asthma and respiratory illness (23). Asthma, the most common chronic disease of childhood, is intimately linked to residential exposures of indoor allergens and pollutants (23-24). Indeed, it has been estimated that over 40% of doctor-diagnosed asthma in children under 16 years is attributable to residential exposures (23-24). In the past 2 decades, asthma rates doubled in U.S. children (25). Finally, a number of agents encountered in housing, including pesticides, have been linked to detrimental effects in children (26). Thus, it is clear that residential hazards are critical determinants of children’s health.

Childhood exposures to residential hazards are antecedents for diseases in adulthood. The detrimental effects of low-level lead exposure on intelligence are irreversible and dramatically reduce opportunities and increase racial inequality (2, 20). Lead poisoning is also associated with cardiovascular disease, premature live births, delinquent behaviors, and an increased mortality from all causes (27). Similarly, exposures to indoor allergens during early childhood are critical for the development of asthma and the consequences of childhood asthma persist throughout life (28). Racial and socioeconomic disparities in environmentally induced diseases, already apparent in childhood, are pronounced (1, 6, 13, 29). Collectively, these data indicate that to protect children from the major causes of morbidity and mortality, it is critical to develop health policy focusing on the control of residential hazards. Many of the strategies and tools that are necessary to protect children from undue lead exposure are relevant to other residential hazards.

A Strategy for the Primary Prevention of Lead Poisoning

A comprehensive strategy for the primary prevention of childhood lead poisoning should include several components.

1. Empirically-Based Residential Lead Standards

Promulgation of empirically-derived, health-based residential lead standards are essential. The lead dust standards would be used to screen housing before a child is unduly exposed, and after lead hazard controls or renovation (8). These standards must be empirically-derived and they must be enforced. Voluntary "standards" are unlikely to protect the majority of children from undue lead exposure.

Screening housing units by using dust samples should be incorporated into housing codes. Dust sampling should be required prior to approval of federal subsidizes for housing. Exceptions could be made for housing units that have been shown to be free of lead-based paint. Screening could be targeted to rental housing because the majority of children who have blood lead levels of 10 m g/dL or higher reside in rental housing.

Studies to assess the ability of individuals who have taken 1-day training programs to accurately measure lead-contaminated house dust are needed. Ongoing research is testing the ability of families to conduct dust sampling for lead. These research projects are essential to make what is generally regarded as the single most important tool to identify housing units that contain lead hazards (i.e., dust wipe samples) more widely available.

2. Strategy to Identify and Target Residential Lead Hazards

National, state and community surveys of housing need to be conducted to identify and prioritize the elimination of residential lead hazards. There should be plans for the identification and remediation of lead-contaminated housing. There should also be plans for the gradual elimination of lead hazards during renovation or demolition of older housing.

3. Studies to Prove Lead Hazard Controls Protect Children

Once residential hazards are identified, it is essential to have safe and effective methods to eliminate them. Although there is good evidence that lead abatement or lead hazard controls are effective in reducing exposure for children who have blood lead levels over 25 m g/dL, there is limited evidence that existing lead hazard controls are safe or efficacious for children with blood lead levels below 25 m g/dL. Evidence of their safety and efficacy must initially rely on children’s blood lead levels. Thereafter, dust lead levels and other environmental measures could be used to evaluate various lead hazard controls. Lead hazard controls need to be assessed in trials that are experimental in design or, at a minimum, include a control group to account for potential confounding variables, such as seasonal variation and the typical decline in children’s blood lead levels as they mature.

An expert committee convened by the National Academy of Sciences should be asked to critically examine what is known about the safety and efficacy of existing lead hazard controls. Specific components of lead hazard controls, such as wet versus dry scraping to remove leaded paint, should be tested. Too often, we have relied on expert opinion about what is safe or effective. These methods can and should be tested in randomized trials. Lower cost interventions should be compared with full abatement in controlled trials.

Various strategies that are ultimately shown to be safe and effective in preventing lead exposure should be allowed. Owners or landlords can then make larger investments for longer term benefits (full abatement) and smaller investments that require ongoing maintenance (lower cost lead hazard controls). This will provide flexibility for housing units with lower and higher value.

 
  1. Scientific Advisory Committee to HUD

A Scientific Advisory Committee should be established to advise the Director of the Office of Lead Hazard Control and Healthy Home Initiative in the U.S. Department of Housing and Urban Development. This committee would advise the Director about research that is necessary to protect children from residential lead hazards, including lead poisoning, asthma, and residential injuries.

Funds to conduct research to improve our understanding of and control efforts for residential hazards (asthma, injuries and lead exposure) should be expanded. These funds should specifically target housing factors related to residentially-induced diseases and be designated to the Centers for Disease Control and U.S. Department of Housing and Urban Development. These funds should be no less than $100 million annually.

5. Establish National Institute for Safe Housing

A national institute for the study and control of housing-related morbidity and mortality in children is needed. This institute should conduct research to understand and control residentially-induced diseases in children. It should maintain surveillance for residentially-induced diseases. It should assess the science underlying standards or recommendations for residential hazards from the CDC, EPA or HUD. It should coordinate efforts of these and other agencies to ensure that vital public health research is conducted.

The research conducted by this Institute should adhere to the principle that passive controls (i.e., efforts that do not require modifying individuals’ behaviors) are the most effective ways to eliminate residentially-induced diseases. For too long, we have simply passed out brochures or told mothers to "clean their houses better" to reduce their child’s risk of lead poisoning. Educational efforts or dust control are inadequate unless lead based paint is made inaccessible.

This Institute should have funds to conduct research and make awards to universities, public health and housing agencies, and other entities for the purpose of understanding and controlling residentially-induced diseases in children.

Summary

The current lead poisoning prevention strategy largely ignores existing scientific evidence indicating that our efforts should emphasize primary prevention. Most federal agencies involved in lead poisoning prevention acknowledge that primary prevention is preferable, yet our efforts continue to focus on screening children for elevated blood lead levels and controlling lead hazards only after a child has been unduly exposed. It is time to establish a scientifically based strategy to eliminate subclinical lead toxicity by controlling residential lead hazards; it is within our grasp.

References

  1. Centers for Disease Control. MMWR 46:141-146. (1997).
  2. Baghurst PA, et al. N Engl J Med 327:1279-1284 (1992); Bellinger D, et al. Pediatrics, 87:219-227 (1991); Bellinger DC, et al. Pediatrics 90:855-861 (1992); Dietrich KN, et al. Pediatrics 91:301-307 (1993); Needleman HL, et al. JAMA 263:673-678 (1990); Needleman HL, et al. N Engl J Med 322:83-88. (1990); Thacker SB, et al. Arch Environ Health 47:336-346. (1992).
  3. Lanphear BP. Science 1998;281:1617-1618.
  4. Centers for Disease Control. Preventing lead poisoning in young children: A statement by the Centers for Disease Control, October 1991, Atlanta, GA: U.S. Public Department of Health and Human Services.
  5. Brody DJ, et al. JAMA 272:277-283. (1994); Hayes EB, et al. Pediatrics 93:195-200. (1994)
  6. Lanphear BP, et al. Pediatrics 101:264-271. (1998); Sargent JD, et al. Am J Public Health 85:528-534. (1995)
  7. Patterson C, et al. Sci Total Environ 1991;107:205-236.
  8. Schwartz J. Environ Res 1994;65:42-55, Schwartz J, et al., Arch Environ Health 1991;46:300-305, Lanphear BP, et al. Public Health Reports 2000;115:521-529.
  9. Bellinger D, Dietrich KN. Pediat Ann 23:600-605. (1994), Lanphear BP, et al. Ped Research 2001;49:16A.
  10. CDC. Screening young children for lead poisoning. Atlanta: CDC, 1997.
  11. Shannon MW, et al. Pediatrics 89:87-90. (1992); McElvaine MD, et al. Pediatrics 89:740-742. (1992). Charney E, et al. Pediatrics 1980; 65:226-231.1980.
  12. Lanphear BP, et al. Am J Public Health 86:1416-1421. (1996); Lanphear BP, et al. Am J Public Health 86:1460-1463. (1996); Clark CS, et al. Environ Res 38:46-53. (1985); Lanphear BP, et al. Environ Res 74:67-73 (1997); Rabinowitz M, et al. Environ Res 38:96-107. (1985); Lanphear BP, et al. Environ Res 1998;79:51-68.
  13. Lanphear BP, et al. Am J Public Health 86:1416-1421. (1996). Lanphear BP, et al. Environ Res 1998;79:51-68, Lanphear BP, et al. Journal of Pediatrics (in press).
  14. Amitai Y, et al. Pediatrics 88:893-897. (1991); Rey-Alvarez S, et al. Pediatrics 79:214-217. (1987); Chisolm JJ. Am J Public Health 26:236-237. (1986); Farfel MR, et al. Am J Public Health 80:1240-1245. (1990); Swindell SL, et al. Clin Pediatrics 536-541. (1994); Aschengrau A, et al. Am J Public Health 87:1698-1702. (1997).
  15. Staes C, et al. Am J Epidemiol 139:1016-1026. (1994); U.S. EPA. 1996, EPA Report 747-R-95-009; Charney E, et al. N Engl J Med 309:1089-1093. (1983).
  16. Aschengrau A, et al. Am J Public Health 87:1698-1702. (1997).
  17. Farfel MR, Chisolm JJ. Am J Public Health 80:1240-1245. (1990). Farfel MR, et al. Environ Res 66:217-221. (1994).
  18. Regulatory Impact Analysis of the Proposed Rule on Lead Based Paint in Federally Owned Residential Property (Office of Lead Hazard Control, Department of Housing and Urban Development, Washington, DC, 1996).
  19. Lanphear BP, et al. Public Health Reports 2000;115:521-529. Lanphear BP, et al. Ped Research 2001;49:16A.
  20. Needleman HL, et al. JAMA 1996;275:363-369, Dietrich KN, et al., Neurotox Teratology (in press), Moss ME, et al., JAMA 1999;281:2294-2298, Schwartz J. Environ Res 1994;66:105-124.
  21. McLoughlin E, et al. Am J Dis Child 1990 144:677-683. Rivara FP, et al. N Engl J Med 1997 Aug 28;337: 543-548, 613-618. Rivara FP, et al. Pediatrics 1993;92:61-63. Stone KE, et al. Journal of Urban Health 2000;77:26-33. Pollack DA, et al. MMWR 1988;37:13-20.
  22. Aligne CA, et al. Arch Pediatr Adolesc Med 1997;151(7):648-653.
  23. Pirkle JL, et al. JAMA 1996 Apr 24;275(16):1233-1240. Gergen PJ, et al. Pediatrics 1998 Feb 1;101(2):E8. Chilmonczyk BA, et al. New Engl J Med 1993;328;1665-1669. Lanphear BP, et al. Pediatrics 2001;017:505-511.
  24. Platt-Mills TAE, et al. J Allergy Clin Immunol 1995;96:435-440. Pope AMR, et al. Indoor Allergens -- Assessing and controlling adverse health effects. 1993,. National Academy Press, Washington, D.C. Taylor W, et al. Pediatrics 1992;90:657-662.
  25. Gergen PJ, et al. JAMA 1990;264:1688-1692. Weiss KB, et al. Ann Rev Publ Health 1993;14:491-513.
  26. Daniels JL, et al. Environ Health Perspect 1997;105:1068-1077. Montana E, et al. Pediatrics 1997 Jan 1;99(1):E5
  27. McDonald JA, et al. Arch Environ Health 1996;51:116-121. Schwartz J. Environ Res 1994;66:105-124. Needleman HL, et al. JAMA 1996;275:363-369 National Research Council. Measuring lead exposure in infants, children, and other sensitive populations. National Academy Press, 1993.
  28. Strachan DP, et al. BMJ 1996;312:1195-1199.
  29. Gold DR, et al. Am Rev Respir Dis 1993;148:10-18.

Home | Menu | Links | Info | Chairman's Page