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Editorial |

Reducing Blood Lead Levels: Title and subTitle BreakBenefits and Strategies

Thomas D. Matte, MD, MPH
JAMA. 1999;281(24):2340-2342. doi:10.1001/jama.281.24.2340
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Despite dramatic reductions in population lead exposure over the past 2 decades, nearly 900,000 US children younger than 6 years still have elevated blood lead levels (≥0.483 µmol/L [≥10 µg/dL]).1 - 2 The problem disproportionately affects low-income children living in older dwellings. Available data suggest that subtle health effects, such as lower IQ scores in children, may extend to blood lead levels well below the 0.483-µmol/L (10-µg/dL) threshold.3 While not as well studied, an association between blood lead levels in this range and cognitive function of middle-aged and elderly men has also been reported.4 Further research may continue to redefine what constitutes an entirely "safe" level.

Much of the reduction in lead exposure to date has come from eliminating uses of lead, such as in gasoline, soldered cans, and housepaint, that were causing widespread, ongoing exposures.5 The opportunity for such relatively simple but powerful interventions has waned as the most hazardous uses of lead have been largely phased out in the United States (although not, unfortunately, in many developing nations). The remaining challenge is far more complex: to address the large reservoirs of lead in paint and exterior soil and dust contaminated from past uses. Some further declines in exposure may occur with turnover in the housing stock and dilution of existing soil and dust contamination. However, without additional efforts to reduce lead hazards at the level of individual homes and neighborhoods, such changes will come too slowly to avoid harm to many cohorts of children.

Consequently, as the distribution of blood lead levels has shifted downward, policy makers and researchers continue to address 2 questions: (1) what impact do blood lead levels prevailing in the population today have on human health; and (2) what interventions can further reduce the risk of lead toxicity, especially among those at highest risk? Two reports in this issue of THE JOURNAL address aspects of these questions.

Moss and colleagues6 add data on dental caries to other findings supporting health effects of lead at levels common in the general population, including lower IQ scores and reductions in stature. Based on data from the Third National Health and Nutrition Examination Survey (NHANES III),7 the authors report a direct relation of blood lead levels in children to the prevalence and extent of dental caries,6 even for levels well below 0.24 µmol/L (5 µg/dL). The authors estimate that variation in lead exposure could account for perhaps 20% or more of the prevalence of dental caries among older children.

In addition to the usual limitations of cross-sectional data, at least 2 caveats should be kept in mind when interpreting these findings. First, it is not clear whether other nutritional or behavioral factors might confound the observed association between lead and caries. The roles of iron8 and ascorbic acid,9 for example, can and should be assessed with data available in NHANES III. In addition, the authors are perhaps too quick to minimize the possibility of potential confounding of their findings by exposure to fluoridated drinking water. Lead exposure is influenced by both individual-level factors and community characteristics (such as urbanization).10 If lead exposure and lack of fluoridation are correlated at the community level, this could explain some of the dental caries risk gradient reported by Moss et al. Despite these limitations, the strength of the relationship reported by Moss et al, its consistency across age groups, and supporting animal data bolster a causal explanation.

The study by Simon and Hudes11 concerns the second question of potential interventions to reduce the risk of lead toxic effects. The authors report an inverse relationship of serum ascorbic acid levels to blood lead levels in both children and adults. As in the study by Moss et al, Simon and Hudes used NHANES III data to examine in the general population an association suggested by animal and limited human data. The association of both high blood lead levels10 and low dietary ascorbic acid intake (in adults) with poverty12 raises the possibility of confounding by socioeconomic status. Since the authors largely addressed this possibility, their results imply that the impact of increasing ascorbic acid intake on blood lead levels could be greatest in the highest-risk populations.

Ascorbic acid intake is but 1 of several nutritional factors that may influence lead toxicity through an influence on absorption, elimination, transport, tissue binding, or secondary mechanisms of toxicity.13 Irregular food intake, high dietary fat intake, low dietary calcium, and iron deficiency can increase the risk of lead toxicity in a contaminated environment.14 As Simon and Hudes point out, however, causal inference from observational studies of isolated nutrient effects is difficult, given the tendency of any nutrient to covary with others and with social or lifestyle factors associated with lead exposure. An additional, unfortunate limitation of this study is the lack of data on the group of greatest interest—children younger than 6 years. Even though a beneficial effect of ascorbic acid supplements on lead levels is supported by a recent report from a small randomized trial in adult smokers,15 more evidence from controlled intervention trials is needed to demonstrate the real value, if any, of increased ascorbic acid intake, especially in young children.

Even if a nutritional manipulation is proven effective in reducing blood lead levels, reliance on such an intervention places most of the burden for prevention on those most affected and least responsible for the underlying environmental causes of lead toxicity.16 Nutritional interventions, therefore, must never substitute for efforts to reduce lead exposure to safe levels. On the other hand, when used as an adjunct to environmental measures, some nutritional changes may prove to have benefits beyond any impact on lead toxicity. For example, studies have suggested benefits of higher ascorbic acid intake on blood pressure,17 blood lipid profiles,18 and respiratory symptoms.19

What needs to be done to hasten the reduction of lead exposure, especially for the populations most affected? While existing efforts, such as screening and responding to lead-poisoned children, need to continue, it would seem reasonable to propose expanded activity on 2 fronts in particular.

First, public and private efforts should be made to increase the testing and remediation of residential lead hazards from deteriorated paint and contaminated dust before children develop lead toxic effects. Interior dust lead measurements, available at relatively low cost, can now be used to help identify the most immediately hazardous dwellings,20 and interventions are available to substantially reduce residential lead exposure.21 The use of this relatively inexpensive test should be expanded, thus decreasing the reliance on elevated blood lead levels in children to identify hazardous home environments.

Second, additional research is needed regarding the sources, fate, and remediation of contaminated exterior dust and soil, which can have major effects on blood lead levels.20 ,22 Approximately 11% of pre-1980 homes are estimated to have soil lead concentrations exceeding 1000 ppm,23 and lead levels in some urban communities may be comparable to those found in communities contaminated by smelting and mining operations.20 Practical interventions and the resources to implement them in large urban areas are currently lacking.

The studies by Moss et al6 and Simon and Hudes11 add to existing knowledge of the benefits of reducing lead exposure and of the potential role of nutrition in augmenting environmental efforts. These reports do not fundamentally alter current understanding of the causes of the remaining lead exposure problem or the actions required for its elimination. Until recently, the perceived scope of the problem—some 57 million pre-1978 private dwelling units are estimated to have at least some leaded paint24 —and its connection to the deeper problems of poverty and substandard housing made its elimination seem an elusive goal. However, by focusing prevention efforts on vulnerable populations exposed to immediate lead hazards, progress toward the virtual eradication of childhood lead toxicity can be greatly accelerated.

REFERENCES

Centers for Disease Control and Prevention.  Preventing Lead Poisoning in Young Children. Atlanta, Ga: Dept of Health and Human Services; 1991.
Centers for Disease Control and Prevention.  Blood lead levels—United States, 1991-1994.  MMWR Morb Mortal Wkly Rep.1997;46:141-146.
Schwartz J. Low-level lead exposure and children's IQ: a meta-analysis and search for a threshold.  Environ Res.1994;65:42-55.
Payton M, Riggs KM, Spiro A, Weiss ST, Hu H. Relations of bone and blood lead to cognitive function: the VA Normative Aging Study.  Neurotoxicol Teratol.1998;20:19-27.
Pirkle JL, Brody DJ, Gunter EW.  et al.  The decline in blood lead levels in the United States—the National Health and Nutrition Examination Surveys.  JAMA.1994;272:284-291.
Moss ME, Lanphear BP, Auinger P. Association of dental caries and blood lead levels.  JAMA.1999;281:2294-2298.
Ballew C, Khan LK, Kaufmann R, Mokdad A, Miller DT, Gunter EW. Blood lead concentration and children's anthropometric dimensions in the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994.  J Pediatr.1999;134:623-630.
Miguel JC, Bowen WH, Pearson SK. Influence of iron alone or with fluoride on caries development in desalivated and intact rats.  Caries Res.1997;31:244-248.
Vaananen MK, Markkanen HA, Tuovinen VJ, Kullaa AM, Karinpaa AM, Kumpusalo EA. Dental caries and mutans streptococci in relation to plasma ascorbic acid.  Scand J Dent Res.1994;102:103-108.
Brody DJ, Pirkle JL, Kramer RA.  et al.  Blood lead levels in the US population: phase 1 of the Third National Health and Nutrition Examination Survey.  JAMA.1994;272:277-283.
Simon JA, Hudes ES. Relationship of ascorbic acid to blood lead levels.  JAMA.1999;281:2289-2293.
Block G, Sorenson A. Vitamin C intake and dietary sources by demographic characteristics.  Nutr Cancer.1987;10:53-65.
Peraza MA, Ayala-Fierro F, Barber DS, Casarez E, Rael LT. Effects of micronutrients on metal toxicity.  Environ Health Perspect.1998;106(suppl 1):203-216.
Mahaffey KR. Nutrition and lead: strategies for public health.  Environ Health Perspect.1995;103(suppl 6):191-196.
Dawson EB, Evans DR, Harris WA, Teter MC, McGanity WJ. The effect of ascorbic acid supplementation on the blood lead levels of smokers.  J Am Coll Nutr.1999;18:166-170.
Hu H, Kotha S, Brennan T. The role of nutrition in mitigating environmental insults: policy and ethical issues.  Environ Health Perspect.1995;103(suppl 6):185-190.
Ness AR, Chee D, Elliott P. Vitamin C and blood pressure—an overview.  J Hum Hypertens.1997;11:343-350.
Simon JA, Hudes ES. Relation of serum ascorbic acid to serum lipids and lipoproteins in US adults.  J Am Coll Nutr.1998;17:250-255.
Schwartz J, Weiss ST. Dietary factors and their relation to respiratory symptoms: the Second National Health and Nutrition Examination Survey.  Am J Epidemiol.1990;132:67-76.
Lanphear BP, Matte TD, Rogers J.  et al.  The contribution of lead-contaminated house dust and residential soil to children's blood lead levels.  Environ Res.1998;79:51-68.
Farfel MR, Chisolm Jr JJ, Rohde CA. The longer-term effectiveness of residential lead paint abatement.  Environ Res.1994;66:217-221.
Bornschein RL, Succop P, Kraft KM, Clark CS, Peace B, Hammond PB. Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment. In: Hemphill DD, ed. Trace Substances in Environmental Health, XX: Proceedings of University of Missouri's 20th Annual Conference, June 1986. Columbia: University of Missouri; 1987:322-332.
Environmental Protection Agency.  Distribution of Soil Lead in the Nation's Housing Stock. Washington, DC: Office of Pollution Prevention and Toxics. Environmental Protection Agency; 1996. Report No. EPA 747-R-96-003.
Department of Housing and Urban Development.  Comprehensive and Workable Plan for the Abatement of Lead-Based Paint in Privately Owned Housing, Report to Congress. Washington, DC: Office of Policy Development and Research; 1990.

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Centers for Disease Control and Prevention.  Preventing Lead Poisoning in Young Children. Atlanta, Ga: Dept of Health and Human Services; 1991.
Centers for Disease Control and Prevention.  Blood lead levels—United States, 1991-1994.  MMWR Morb Mortal Wkly Rep.1997;46:141-146.
Schwartz J. Low-level lead exposure and children's IQ: a meta-analysis and search for a threshold.  Environ Res.1994;65:42-55.
Payton M, Riggs KM, Spiro A, Weiss ST, Hu H. Relations of bone and blood lead to cognitive function: the VA Normative Aging Study.  Neurotoxicol Teratol.1998;20:19-27.
Pirkle JL, Brody DJ, Gunter EW.  et al.  The decline in blood lead levels in the United States—the National Health and Nutrition Examination Surveys.  JAMA.1994;272:284-291.
Moss ME, Lanphear BP, Auinger P. Association of dental caries and blood lead levels.  JAMA.1999;281:2294-2298.
Ballew C, Khan LK, Kaufmann R, Mokdad A, Miller DT, Gunter EW. Blood lead concentration and children's anthropometric dimensions in the Third National Health and Nutrition Examination Survey (NHANES III), 1988-1994.  J Pediatr.1999;134:623-630.
Miguel JC, Bowen WH, Pearson SK. Influence of iron alone or with fluoride on caries development in desalivated and intact rats.  Caries Res.1997;31:244-248.
Vaananen MK, Markkanen HA, Tuovinen VJ, Kullaa AM, Karinpaa AM, Kumpusalo EA. Dental caries and mutans streptococci in relation to plasma ascorbic acid.  Scand J Dent Res.1994;102:103-108.
Brody DJ, Pirkle JL, Kramer RA.  et al.  Blood lead levels in the US population: phase 1 of the Third National Health and Nutrition Examination Survey.  JAMA.1994;272:277-283.
Simon JA, Hudes ES. Relationship of ascorbic acid to blood lead levels.  JAMA.1999;281:2289-2293.
Block G, Sorenson A. Vitamin C intake and dietary sources by demographic characteristics.  Nutr Cancer.1987;10:53-65.
Peraza MA, Ayala-Fierro F, Barber DS, Casarez E, Rael LT. Effects of micronutrients on metal toxicity.  Environ Health Perspect.1998;106(suppl 1):203-216.
Mahaffey KR. Nutrition and lead: strategies for public health.  Environ Health Perspect.1995;103(suppl 6):191-196.
Dawson EB, Evans DR, Harris WA, Teter MC, McGanity WJ. The effect of ascorbic acid supplementation on the blood lead levels of smokers.  J Am Coll Nutr.1999;18:166-170.
Hu H, Kotha S, Brennan T. The role of nutrition in mitigating environmental insults: policy and ethical issues.  Environ Health Perspect.1995;103(suppl 6):185-190.
Ness AR, Chee D, Elliott P. Vitamin C and blood pressure—an overview.  J Hum Hypertens.1997;11:343-350.
Simon JA, Hudes ES. Relation of serum ascorbic acid to serum lipids and lipoproteins in US adults.  J Am Coll Nutr.1998;17:250-255.
Schwartz J, Weiss ST. Dietary factors and their relation to respiratory symptoms: the Second National Health and Nutrition Examination Survey.  Am J Epidemiol.1990;132:67-76.
Lanphear BP, Matte TD, Rogers J.  et al.  The contribution of lead-contaminated house dust and residential soil to children's blood lead levels.  Environ Res.1998;79:51-68.
Farfel MR, Chisolm Jr JJ, Rohde CA. The longer-term effectiveness of residential lead paint abatement.  Environ Res.1994;66:217-221.
Bornschein RL, Succop P, Kraft KM, Clark CS, Peace B, Hammond PB. Exterior surface dust lead, interior house dust lead and childhood lead exposure in an urban environment. In: Hemphill DD, ed. Trace Substances in Environmental Health, XX: Proceedings of University of Missouri's 20th Annual Conference, June 1986. Columbia: University of Missouri; 1987:322-332.
Environmental Protection Agency.  Distribution of Soil Lead in the Nation's Housing Stock. Washington, DC: Office of Pollution Prevention and Toxics. Environmental Protection Agency; 1996. Report No. EPA 747-R-96-003.
Department of Housing and Urban Development.  Comprehensive and Workable Plan for the Abatement of Lead-Based Paint in Privately Owned Housing, Report to Congress. Washington, DC: Office of Policy Development and Research; 1990.
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