(May 1992)
Table of Contents
Acknowledgement
Foreword
Introduction
Populations at
risk
Sources of lead
exposure
Extent of lead
poisoning in children
Soil
characterization
Particle size
and lead content of house dust
Environmental
fate of lead
Bioavailabilty
of lead
Metabolic
interactions of lead with nutrients
Health effects
of lead exposure
References
Figures
Point of contact
for this document:
This document was downloaded from the CDC Prevention Guidelines on the WWWonder database and reformatted. The author of the report thanks the CDC staff responsible for the HTML coding of the original paper.
Special recognition is due the various ATSDR staff personnel who reviewed and critiqued drafts of this document, and who suggested changes to the text, many of which strengthened and clarified the final version. Among those individuals contributing to this paper, of particular note is Dr. Kenneth Orloff, Assistant Director for Science, Division of Health Assessment and Consultation, whose initial draft background paper on lead in soil formed the point of departure for the present document. Special thanks are due to the members of the ATSDR Science Forum for their many constructive criticisms of successive drafts and to the staff of the ATSDR Visual Information Center for their contribution on graphic design and typesetting. Ms. Jeanne Bucsela served as editor.
Lead in the environment and its effects on the health of people is a matter
of great concern to the Agency for Toxic Substances and Disease Registry
(ATSDR). The Agency was established by the Comprehensive Environmental Response,
Compensation, and Liability Act of 1980 (CERCLA, also known as Superfund) to
assess the public health impact of hazardous wastes in the general environment,
to identify human populations at risk, and to effect actions to prevent adverse
health effects from human contact with hazardous substances. The Agency's
emphasis is on hazardous substances released from waste sites and substances
released under emergency conditions (e.g., chemical spills). Lead left in the
environment as hazardous waste is a matter of great public health concern to
ATSDR.
ATSDR's concern about lead's toxicity derives from several factors. In a
report to Congress, The Nature and Extent of Lead Poisoning in Children in the
United States, published by ATSDR in July 1988, exposure to lead was identified
as a serious public health problem, particularly for children. The report also
identified six major environmental sources of lead, including leaded paint,
gasoline, stationary sources, dust/soil, food, and water. For leaded paint, the
number of potentially exposed children under 7 years of age in all housing with
some lead paint at potentially toxic levels is about 12 million. An estimated
5.6 million children under 7 years old are potentially exposed to lead from
gasoline at some level. The estimated number of children potentially exposed to
U.S. stationary sources (e.g. smelters) is 230,000 children. The range of
children potentially exposed to lead in dust and soil is estimated at 5.9
million to 11.7 million children. Some actual exposure to lead occurs for an
estimated 3.8 million children whose drinking water lead level has been
estimated at greater than 20 mcg/dl.
CERCLA requires ATSDR and the Environmental Protection Agency (EPA) to
jointly rank, in order of priority, hazardous substances found at sites on EPA's
National Priorities List (NPL). The current list of prioritized hazardous
substances numbers 275. The three criteria for ranking were frequency of
occurrence at NPL sites, toxicity, and potential for human exposure. Lead is
ranked as the number one priority hazardous substance. In view of this, exposure
to lead in populations close to hazardous waste sites continues to be a public
health issue of concern. ATSDR, in reaction to this concern, recently
established a Lead Initiative to systematically review Superfund sites for which
the Agency's Public Health Assessments indicate the presence of site-related
lead contamination. The goal of this ATSDR initiative is to prevent lead
toxicity in persons, especially young children, exposed to lead released from
Superfund sites and facilities. For all sites on the NPL, lead occurred at 853
(66%) of the 1300 sites. Thirteen sites have been selected for in-depth
follow-up in fiscal year 1992 by ATSDR scientists.
This report provides background information on the complex and interactive
factors that environmental health scientists need to consider when evaluating
the impact of lead-contaminated soil on public health. A definitive analysis of
the impact on public health of lead-contaminated soil is limited often by a lack
of information on human exposure factors and soil conditions. Each waste site,
therefore, poses a unique challenge to the health assessor and each site should
be assessed in terms of its own characteristics.
The development of action levels for lead in soil lies outside the scope of
the present report. However, the health assessor will find the information in
this report useful in characterizing the significance of exposure pathways and
the importance of the physical and chemical properties of the lead compounds
that may impact on persons' uptake of lead.
The correlation between lead-contaminated soil and blood lead (PbB) level
continues to challenge investigators. Correlations cited in the literature are
influenced in specific studies by many factors, including access to soil,
behavior patterns (especially of children), presence of ground cover, seasonal
variation of exposure conditions, particle size and composition of the lead
compounds found at various sites and the exposure pathway. These complex factors
explain in some instances discrepant findings that are reported in the
literature.
The reader is cautioned that much research is ongoing to clarify
relationships between lead in soil and the amount absorbed by humans. Therefore,
the associations and mathematical relationships between soil lead concentrations
and blood-lead levels cited in this paper should be understood as being what has
been published in the scientific literature, but subject to change as newer
information becomes available.
Barry L. Johnson, Ph.D.
The Agency for Toxic Substances and Disease Registry (ATSDR) is mandated by
the Comprehensive Environmental Response, Compensation, and Liability Act of
1980 (CERCLA or Superfund), as amended by the Superfund Amendments and
Reauthorization Act of 1986 (SARA), to perform public health assessments for all
sites on the National Priorities List (NPL). Data from health assessments for
the first 951 sites show that metals and volatile organic compounds were the
contaminants most often detected, and these commonly migrated from disposal
areas to groundwater. Metallic substances occurred at 564 (59%) of the 951
sites, with lead, chromium, arsenic, and cadmium being cited most frequently
(Susten, 1990).
The purpose of this analysis paper is to examine the relationship between
exposure to lead-contaminated soil and the resulting impact on public health.
The analysis will provide background information to ATSDR staff and other
environmental health scientists responsible for preparing ATSDR documents, such
as health assessments, health consultations, and emergency responses.
Emphasis in the analysis is given to the public health aspects of soil lead
contamination at field sites. The analysis includes a review of the following
areas: populations at high risk, sources of lead exposure, extent of lead
poisoning in children, soil characterization, environmental fate of lead,
bioavailability of lead, health effects of lead poisoning, correlations of soil
lead and blood lead (PbB) in children, soil lead standards and recommendations,
public health impact of exposure to lead-contaminated soil, general principles
and limitations in field evaluations, and community prevention activities.
The Centers for Disease Control (CDC) Lead Statement for Preventing Lead
Poisoning in Young Children is highlighted and provides guidelines on blood lead
levels and childhood lead poisoning prevention (CDC, 1991). Examples in the use
of the EPA Uptake/Biokinetic Model (Version 0.5) for estimating PbB levels from
multiple exposure pathways are included.
Data gaps, such as usage patterns and soil condition, that limit a definitive
analysis on the impact of soil on public health are discussed to the extent that
information is available. Therefore, the development of action levels for lead
in soil lies outside the scope of this document. Interactive and complex factors
associated with multiple exposure pathways for lead require a site-specific
approach in order to develop meaningful action levels for lead in soil.
Identification and discussion of soil remediation protocols are also not within
the scope of this analysis.
Preschool-age children and fetuses are usually the most vulnerable segments
of the population for exposures to lead (ATSDR, 1988). This increased
vulnerability results from a combination of factors including: 1) the developing
nervous system of the fetus or neonate has increased susceptibility to the
neurotoxic effects of lead; 2) young children are more likely to play in dirt
and to place their hands and other objects in their mouths, thereby increasing
the opportunity for soil ingestion (pica--the eating of dirt and other non-food
items--is more likely to occur in children); 3) the efficiency of lead
absorption from the gastrointestinal tract is greater in children than in
adults; and 4) nutritional deficiencies of iron or calcium, which are prevalent
in children, may facilitate lead absorption and exacerbate the toxic effects of
lead.
Among children, those in the 2-3 year-old age bracket may be most at risk for
exposure to lead-contaminated soil. Mahaffey et al. (1982) reported that
children in this age group had the highest PbB concentrations. This is also the
age group in which pica tendencies are most prevalent (ATSDR, 1988).
Several major sources of lead exposure have been identified (ATSDR, 1988).
Leaded paint continues to cause most of the severe lead poisoning in children in
the United States. It has the highest concentration of lead per unit of weight
and is the most widespread of the various sources, being found in approximately
21 million pre-1940 homes. Dust and soil lead--derived from flaking, weathering,
and chalking paint--plus airborne lead fallout and waste disposal over the
years, are the major proximate sources of potential childhood lead exposure.
Lead in drinking water is intermediate but highly significant as an exposure
source for both children and the fetuses of pregnant women. Food lead also
contributes to exposure of children and fetuses.
Individuals may be exposed to lead through several sources. When evaluating a
site, a health assessor should be aware of multiple sources of lead exposure and
the additive nature of the risks. An important source of lead exposure in older
homes is contact with interior or exterior surfaces that have been painted with
lead-based paints. Some individuals may be exposed to lead from occupational or
hobby sources or from other less-common sources, such as the use of lead-glazed
pottery, stained glassworking, and target practice in poorly ventilated indoor
firing ranges.
The 1988 Agency for Toxic Substances and Disease Registry (ATSDR) report on
the extent of lead poisoning in the United States estimated that in the 1984
standard metropolitan statistical areas 2.4 million white and black children
aged 6 months through 5 years had PbB levels above 15 mcg/dl and 200,000
children above 25 mcg/dl. This would correspond to approximately 3 million and
250,000, respectively, for all children 6 months through 5 years in the total
U.S. population.
The actual number of children exposed to lead in dust and soil at
concentrations adequate to elevate PbB levels cannot be estimated with the data
now available. However, the number of children potentially exposed to lead in
dust and soil can be stated as a range of potential exposures to the primary
sources of lead in dust and soil, namely, paint lead and atmospheric lead
fallout. This range is estimated at 5.9 to 11.7 million children (ATSDR, 1988).
Foreword
Assistant Surgeon General
Assistant
Administrator
Introduction
Populations at risk
Sources of lead exposure
Extent of lead poisoning in children
Size range (µm) | Weight % of fractionated dust | Lead content µgPb/g of dust fraction | % Lead in unfractionated dust |
---|---|---|---|
‹44 | 18 | 1440 | 21 |
44-149 | 58 | 1180 | 56 |
149-177 | 4.5 | 1330 | 4.9 |
177-246 | 2.7 | 1040 | 2.3 |
246-392 | 6.1 | 1110 | 5.6 |
392-833 | 11 | 1090 | 9.6 |
Unfractionated Dust | 100 | 1214 ± 13ª | 100 |
Element / Compound | Solubility | |
---|---|---|
Water | Organic solvents | |
Lead | Insoluble | Insoluble |
Lead acetate | 221g/100ml at 50°C | Soluble in glycerol, very slight in alc. |
Lead chloride | 0.99 g/100ml at 20°C | Insoluble in alcohol |
Lead chromate | 0.2 mg/L | Insoluble in acetic acid |
Lead nitrate | 37.65-56.5 g/100ml at 0°C | 1 g in 2,500 ml absolute alcohol 1 g in 75 ml absolute methanol |
Lead oxide | 0.001 g/100 cc at 20°C (Litharge) 0.0023 g/100 cc at 23°C (Massicot) |
Soluble in alkali chlorides Soluble in alkali (Massicot) |
Lead sulfate | 42.5 mg/L at 25°C | Insoluble in alcohol |
Soil: Paint is a major contributor to soil lead contamination. Remediation of exterior lead-based paint hazards is critical if further contamination is to be avoided (Binder and Matte, 1992). The accumulation of lead in soil is primarily a function of the rate of deposition from the atmosphere. The fate of lead in soil is affected by the specific or exchange adsorption at mineral interfaces, the precipitation of sparingly soluble solid phases, and the formation of relatively stable organo-metal complexes or chelates with the organic matter in soil (EPA, 1986; NSF, 1977).
Evidence exists that atmospheric lead enters the soil as lead sulfate or is converted rapidly to lead sulfate at the soil surface. Lead sulfate is relatively soluble, and thus could leach through the soil if it were not transformed. In soils with pH of > or = 5 and with at least 5% organic matter, atmospheric lead is retained in the upper 2-5 cm of undisturbed soil (EPA, 1986).
Lead may mobilize from soil when lead-bearing soil particles run off to surface waters during heavy rains. Lead may also mobilize from soil to atmosphere by downwind transport of smaller lead- containing soil particles entrained in the prevailing wind (NSF, 1977). This latter process may be important in contributing to the atmospheric burden of lead around some lead-smelting and Superfund sites that contain elevated levels of lead in soil.
The downward movement of lead from soil by leaching is very slow under most natural conditions (NSF, 1977). The conditions that induce leaching are the presence of lead in soil at concentrations that either approach or exceed the sorption capacity of the soil, the presence in the soil of materials that are capable of forming soluble chelates with lead, and a decrease in the pH of the leaching solution (e.g., acid rain) (NSF, 1977). Partial favorable conditions for leaching may be present in some soils near lead- smelting and NPL sites that contain elevated levels of lead in soil.
Lead compound | Percent absorption compared with lead acetate |
---|---|
Control (no lead) | 4 |
Metallic lead (particle size 180-250 µm) |
14 |
Lead chromate | 44 |
Lead octoate | 62 |
Lead naphthenate | 64 |
Lead sulfide | 67 |
Lead tallate | 121 |
Lead carbonate (basic) | 164 |
A key factor in the solubility of lead is the pH of the fluid. Healy et al. (1982) measured the solubility of lead sulfide (particle size approximately 90 mcm) in several fluids, including water, saliva, and gastric juice. The lead was relatively insoluble in water and saliva, but was 800 times more soluble in simulated gastric juice. Day et al. (1979) measured the solubility (extractability) in hydrochloric acid of lead from street dust collected in two industrial cities. The authors assumed that the lead compounds were primarily oxides and halides emitted from automobiles. Under environmental conditions, these compounds can be converted to carbonates and sulfates. Less than 10% of the lead was extracted at pH 4 and higher; more than 80% was extracted at pH 1, the nominal pH of gastric juice. The significance of these findings is not clear because the temperature of extraction did not correspond to physiological conditions (37 C) and hydrochloric acid is a simplistic simulation of gastric juice. Other studies have supported the higher degree of solubilization at a pH about 1 of lead from street dust samples (Duggan and Williams, 1977; Harrison, 1979).
The main conclusion to be drawn from studies of lead-nutrient interactions is
that defects in nutrition will enhance lead absorption and retention and thus
the toxicity risk. This problem is amplified when nutrient deficiencies are
commonplace and lead exposure is highest, that is, in 2-to 4- year-old,
underdeveloped children (ATSDR, 1988).
Improving the nutritional status of children who have a high risk of exposure
and toxicity greatly increases the effectiveness of environmental lead
abatement. However, nutritional supplement (calcium) only increases the lead
level required for toxicity rather that eliminating lead uptake and its effects
(Mahaffey, 1982).
The levels of phosphorus, which indicate Vitamin D levels, suggest that most
poor children's intake of this vitamin is adequate (ATSDR, 1988). Vitamin D
enhances lead uptake in the gut, but its intake is essential to health and
cannot be reduced (ATSDR, 1988).
Studies on the effects of lead in children have demonstrated a relationship
between exposure to lead and a variety of adverse health effects. These effects
include impaired mental and physical development, decreased heme biosynthesis,
elevated hearing threshold, and decreased serum levels of vitamin D (Figure 1). The
neurotoxicity of lead is of particular concern, because evidence from
prospective longitudinal studies has shown that neurobehavioral effects, such as
impaired academic performance and deficits in motor skills, may persist even
after PbB levels have returned to normal (Needleman, 1990). Although no
threshold level for these effects has been established, the available evidence
suggests that lead toxicity may occur at PbB levels of 10-15 mcg/dl or possibly
less (ATSDR 1988).
Additional information on lead toxicity is contained in The Nature and Extent
of Lead Poisoning in Children in the United States: A Report to Congress (ATSDR,
1988) and the ATSDR Toxicological Profile for Lead (ATSDR, 1992).
Every community and every study reflects a different range of soil lead
concentrations and blood lead levels. Several comprehensive reviews have
examined the quantitative relationship between exposure to lead-contaminated
soil and PbB levels in children. This result is commonly expressed in the
literature as a dose- response relationship and reflects a change in PbB levels
with the change in soil lead concentrations (assuming a linear relationship
between the two) scaled to a standard unit of soil lead concentration (either
1,000 mcg/g or 100 mcg/g) (Reagan and Silbergeld, 1989).
Duggan compiled data from published studies that reported a quantitative
correlation between PbB concentrations and lead concentrations in soil or dust
(Duggan, 1980; Duggan and Inskip, 1985). Duggan included data from sites with
diverse sources of lead contamination (e.g., lead mining, smelting, lead paint,
automobile exhaust emissions). The data indicated that the increase in PbB
levels associated with exposures to lead in soil varied between 0.6 and 65 mcg
lead/dl blood per 1000 ppm lead in soil. As an average value, Duggan suggested
that exposure to soil containing 1000 ppm of lead could increase the PbB level
by 5 mcg/dl. No value for an acceptable concentration of lead in soil was
offered because such a value would depend on what constitutes an acceptable
increase in the PbB concentration.
In the ATSDR document, The Nature and Extent of Lead Poisoning in Children in
the United States: A Report to Congress, it was noted that several
investigations have shown a highly significant correlation between PbB levels
and lead concentrations in dust and soil. Several references were cited that
describe quantitative relationships between PbB levels and soil or dust lead
levels. The report concluded, "In general, lead in dust and soil at levels of
500 to 1,000 ppm begins to affect children's PbB levels."
Metabolic interactions of lead with nutrients
Mahaffey and
co-workers (1976) reported that children with elevated PbB had lower dietary
intakes of calcium and phosphorus than did a reference population. Heard and
Chamberlain (1982) reported similar findings. Several studies have shown a
strong inverse correlation between iron status and PbB (Chisolm,1981; Yip et
al., 1981; Watson et al., 1980). Zinc deficiency can also enhance lead
absorption (Markowitz and Rosen, 1981).
Health effects of lead exposure
Correlations of soil lead and blood lead in children
Duggan (1980), Duggan and Inskip (1985)
ATSDR (1988)
Study² | Dose response relationships¹ | |
---|---|---|
Change in blood Pb per 1000 µg/g soil lead |
Change in blood Pb per 100µg/g soil lead | |
Urban communities | ||
Angle and McIntire (1982) | 15.5* | 1.6 |
Brunekreef et al. (1983) | 11.3* | 11.1 |
Stark et al. (1982) | 10.2* | 1.0 |
Davies et al. (1987) | 10.0 | 1.0 |
Haan (personal communication) | 10.0 | 1.0 |
Madhaven et al. (1989) | 9.0 | .9 |
Reeves et al. (1982) | 8.1* | 0.8 |
Rabinowitz et al. (1985) | 8.0 | .8 |
Bornschein (1986) | 6.2 | 0.6 |
Shellshear et al. (1975) | 3.9* | 0.4 |
Lead industries communities | ||
Brunekreef et al. (1981) | 12.6* | 1.3 |
Landrigan et al. (1975) | 11.7* | 1.2 |
Neri et al. (1978) | 11.2* | 1.1 |
Yankel et al. (1977) | 7.3* | 0.7 |
Roberts et al. (1974) | 5.3* | 0.5 |
Galke et al. (1975) | 4.9* | 0.5 |
Mining communities | ||
Gallacher et al. (1974) | 4.1 | 0.4 |
Barltrop et al. (1974) | 0.6* | 0.1 |
Review articles | ||
Brunekreef et al. (1986) | 5-10 | 0.5-1.0 |
AAP (1987) | 5-10 | 1.0-2.0³ |
Duggan (1980, 1983) | 5 | 0.5 |
EPA (1986a) | 2 | 0.2 |
¹ This table reflects unadjusted values (calculated by Brunekreef (1986)
and
noted by an * and values in other studies calculated by the authors of
the study.
² See Reagan and Silbergeld (1989) for full citations for these
references.
³ Covering the range of 500-1,000 µg/g only.
Reagan and Silbergeld (1989) analyzed the review articles by Brunekreef (1986), American Academy of Pediatrics (AAP) (1987), Duggan (1980), Duggin and Inskip (1985), and EPA (1986) and reported several limitations in the articles. In the Brunekreef review, most studies reviewed "do not permit straightforward calculation of (a dose-response relationship) which are properly adjusted for relevant confounders". Nevertheless, Brunekreef concluded that the dose-response relationship was in the 5.0-10.0 (mcg/dl per 1,000 mcg/g) range for lead in soil, housedust, streetdust, and playground dust. After reviewing several studies Duggan also concluded that the dose-response relationship of PbB to soil lead concentration is 5 mcg/dl per 1000 mcg/g which is very close to his theoretical calculation of 7 mcg/dl per 1,000 mcg/g. Brunekreef criticized Duggan's review because he relied heavily on studies in which one or more pathways were excluded and used adjusted instead of unadjusted values in some studies.
The review by the AAP notes that for each increase of 100 mcg/g in the lead content of surface soil above a level of 500 mcg/g a mean increase of 1 to 2 mcg/dl occurs in children's whole PbB (AAP 1987). No explanation was given in the AAP study for starting the slope at a soil lead value of 500 mcg/g. Reagan and Silbergeld (1989) also criticized the EPA review for selecting only two studies (Stark et al., 1982; Angle and McIntire, 1982), which
EPA believed provided good data for the slope estimates (2.2 mcg/dland 6.8 mcg/dl) and then selecting the lowest one as a "median estimate" without explaining why this selection technique is appropriate. Brunekreef also criticized the EPA conclusion because EPA mixed adjusted and unadjusted values and because use of an adjusted value in the Stark study was inappropriate.
The dose-response relationship differs between urban and industrial communities and lead-mining communities, with lead-mining communities having a shallower slope (Reagan and Silbergeld, 1989). This difference is probably due to a difference in the bioavailabilty of lead. Particle size and metal species are also thought to be major factors (Colorado Department of Health, 1990). However, differences in modulating factors (such as nutrition) may also have been important in these studies.
With regard to particle size, leaded gasoline, which is the predominant source of lead in urban communities, and industrial point sources emit small particles, whereas mines and tailing piles release relatively large particles, primarily as fugitive dusts (EPA, 1986). Smaller particles may be inhaled and ingested, increasing total exposure. Smaller particles are easily transferred to the hands and tend to remain on the hands longer, thereby increasing the potential for ingestion.
With respect to metal species, Steele et al. (1990) noted that the impact of lead in soil derived from mine waste (usually in the form of PbS) on blood lead is less than that for lead in soil derived from smelter, vehicle, or point sources. However, in an animal study, tailing material from Midvale, Utah, was found to be more available to young pigs than was reagent grade PbS when presented as a single large dose by intubation (LaVelle et al. 1991). This study does not lend support to the Steele finding.
The U.S. Environmental Protection Agency (EPA) recently developed an
Integrated Uptake/Biokinetic (IU/BK) model that examines the relationship
between environmental exposure to lead and PbB levels. Examples in the use of
this EPA model (Version 0.5) are shown in (Figure 2), (Figure 3), (Figure 4). This model
is not used to set clean-up standards per se. Rather, it allows the health
assessor to make site-specific calculations for children 6 yrs of age and under
for PbB levels resulting from exposures to lead in soil, dust, air, water, and
the diet. Several assumptions and default exposure variables are built into the
model for use when these parameters are not known. The model is still being
validated by the EPA.
Environmental Protection Agency (1990)
Location | Residential |
---|---|
U.S. (2,3,4) | 500 (a) |
Minnesota (4,5) | 500 (b) |
OME, Canada (2,6) | 375 (c) 500 (d) |
Netherlands (9) | 50 (f) 150 (g) 600 (h) |
England (8,10) | 500 (i) |
London | 500 (j) |
(a) 600 µg/g repealed, changed to leachate standard,
interim 500 µg/g
guideline
(b) proposed emergency rule, interim 1000 µg/g standard
(c)
sandy soil
(d) non-sandy soil
(f) reference value
(g) further
investigation
(h) clean up value
(i) redevelopment of industrial
lands
(j) dust standard
Sources cited (see Reagan and Silbergeld, 1989, for full citations): (2) Rinne et al. (1986); (3) Office of Solid Waste and Emergency Response (OSWER) (1989); (4) personal communication; (5) Minnesota Hazardous Waste Regulations; (6) Ontario Ministry of the Environment (OME) (1986); (8) Davies and Wixson (1986); (9) Assink and Vanderbrink (1986); (10) Department of the Environment (DOE,UK,1987); (11) Wilson (1983).
Researchers have also calculated "acceptable" levels of lead in soil or dust (Table 6).
Author(s) | Standard (ppm) | Comments |
---|---|---|
Shelshear et al. (1975) | <100 | Protect pica children |
Mielke et al. (1989) | <150 | Prevent lead toxicity (10 µg/dl |
Chaney et al. (1986, 1989) | <150 | Protect pica children |
Duggan and Williams (1977) | 300 | Keep ADI <50 µg/Pb/day (street dust standard) |
Boucier et al. (1985) | 300 | Keep blood lead below 25 µg/dl |
Simms and Becket (1987) | 500 | Keep blood lead below 25 µg/dl |
Madhaven et al. (1989) | 600 250 |
Permit an increase in blood lead of 5 µg/dl above existing
levels Protect children where there is no grass cover |
Steenhout (1987) | 900 | Based upon an ADI of 200 µg Pb/day |
Laxen et al. (1987) | 1000 | Allows dust to contribute 2.5-3.0 µg/dl (housedust) |
Reagan and Silbergeld (1989) also noted an order of magnitude difference in the recommendations offered in the literature. The standards reflect four basic arguments to justify or advocate a specific lead limitation.
Author(s) | Recommended standard (ppm) | Normalized (ppm) |
---|---|---|
Shelshear et al. (1975) | <100 | <100 |
Mielke et al. (1989) | <150 | <150 |
Chaney et al. (1986, 1989) | <150 | <150 |
Duggan and Williams (1977) | 300 | 150 |
Boucier et al. (1985) | 300 | 120 |
Simms and Becket (1987) | 500 | 200 |
Madhaven et al. (1989) | 600 250 |
120 50 |
Steenhout (1987) | 900 | 112 |
Laxen et al. (1987) | 1000 | 333 |
In recommending a soil lead standard, Reagan and Silbergeld argue that
Finally, Reagan and Silbergeld argue "that the literature as a whole supports a low soil lead standard of 100 mcg/g or so." In proposing this standard, Reagan and Silbergeld (1989) also proposed that the standard:
Class | Blood lead concentration (µg/dl | Comment |
---|---|---|
I | = or < 9 | A child in Class I is not considered to be lead- poisoned |
IIA | 10-14 | Many children (or a large proportion of children) with blood lead levels in this range should trigger community-wide childhood lead poisoning prevention activities. Children in this range may need to be screened more frequently. |
IIB | 15-19 | A child in Class IIB should receive nutritional and educational interventions and more frequent screening. If the blood lead levels persist in this range, environmental investigation and intervention should be done. |
III | 20-44 | A child in Class III should receive environmental evaluation and remediation and a medical evaluation. Such a child may need pharmacologic treatment of lead poisoning. |
IV | 45-69 | A child in Class IV will need both medical and environmental interventions, including chelation therapy. |
V | = or > 70 | A child in Class V lead poisoning is a medical emergency. Medical and environmental management must begin immediately |
(Adapted from CDC, Preventing Lead Poisoning in Young Children. A Statement by the Centers for Disease Control, October, 1991. U.S. Department of Health aand Human Services/Public Health Service) If PbB levels are elevated, exposure to lead-contaminated soil may not be the only source for the increased blood level. Other lead sources - -such as lead from food, water, or air--could be partially or primarily responsible for the elevated PbB. These other potential exposure pathways should be thoroughly evaluated.
Even if PbB levels are not elevated, the site should not be dismissed as posing no potential public health hazard. Potential seasonal variation of exposure conditions; the half-life of lead in the blood stream; and limitations of any screening methods used, especially study design (power and representativeness of blood and soil samples), should be evaluated. If conditions at a site change dramatically, retesting exposed individuals may be necessary to determine the impact of altered conditions on PbB levels. Commonplace changes may also be significant in altering PbB levels.
The results of occupational studies indicate that increased exposures to lead are followed by elevations in PbB levels, which reach a new level in 60-120 days (Tola et al. 1973). Also, PbB levels may be higher in children during the summer months presumably as the result of increased opportunity for exposures through outdoor play.
The biologic fate of inorganic lead in the human body is well known. Inorganic lead is not metabolized but is directly absorbed, distributed, and excreted. Once in the blood, lead is distributed primarily among three compartments--blood, soft tissue (kidney, bone marrow, liver, and brain), and mineralizing tissue (bones and teeth). Mineralizing tissue contains about 95% of the total body burden of lead in adults (ATSDR, 1990).
In blood, 99% of the lead is associated with erythrocytes; the remaining 1% is in the plasma and is available for transport to the tissues. In single-exposure studies with adults, lead has a half- life in blood of approximately 25 days; in soft tissue, about 40 days; and in the non-labile portion of bone, more than 25 years. In bone there is both a labile component, which readily exchanges lead with the blood, and an inert pool. Lead in the inert pool poses a special risk because it is a potential endogenous source of lead. Because of these mobile lead stores, a person's PbB level can take several months or sometimes years to drop significantly, even after complete removal from the source of lead exposure (ATSDR, 1990).
In Leadville, Colorado, the Colorado Department of Health examined the impact of residential soil lead contamination on the PbB levels of children (Colorado Department of Health, 1990). Lead smelting operations in the area ended in 1961, and, at the time of the study in 1987, only one lead and zinc mine was still operating. An increase in soil lead concentration from 100 to 1100 ppm was associated with an estimated increase of 3.9 mcg/dl in the PbB concentration.
The results of several studies have indicated that the increase in PbB concentration as a function of soil lead concentration is not linear. That is, at higher lead concentrations in soil, the rate of increase in PbB levels falls off. Using data from exposure studies conducted at Helena Valley in Montana and Silver Valley in Idaho, Schilling and Bain (1989) derived the following linear regression model for the correlation between PbB levels and soil lead levels:
Using this equation, an increase in soil lead from 100 ppm to 1100 ppm would increase the predicted PbB level from 7.3 mcg/dl to 13.0 mcg/dl, an increase of 5.7 mcg/dl. A further increase in soil lead to 2100 ppm would increase the estimated PbB level to only 15.2 mcg/dl.
The non-linearity of the dose-response curve for blood lead vs. soil lead is not unique to soil lead exposures. The rate of increase in PbB levels has also been observed to decrease upon exposure to high concentrations of lead in air or drinking water (Hammond, 1982).
Under the Superfund Amendments and Reauthorization Act of 1986, EPA (1991) initiated a "pilot program for the removal, decontamination, or other actions with respect to lead-contaminated soil in one to three metropolitan areas". One study, the Three City Urban Soil-Lead Demonstration Project, was designed to investigate whether the use of low-technology abatement methods to reduce environmental lead concentrations (soil, dust) would result in decreased PbB levels in children. Findings from this study are expected in the summer of 1992. It is possible that the impact of contaminated soil, like that of paint, is highly dependent on condition and usage patterns. This issue has not been adequately evaluated (Binder and Matte, 1992).
Screening tests
The erythrocyte protoporphyrin level is not sensitive enough to identify
children with elevated PbB levels below about 25 mcg/dl. The screening test of
choice is now PbB measurement (CDC 1991).
Dose-response curve
When assessing the public health impact of environmental lead contamination,
the lower portion of the dose-response curve for PbB vs. soil lead should be
used. This portion of the curve has the steepest slope, and it corresponds to
conditions in which the impact on PbB is the greatest.
PbB levels generally rise 3-7 mcg/dl for every 1,000-ppm increase in soil or
dust lead concentrations (CDC 1991). Access to soil, behavior patterns, presence
of ground cover, seasonal variation of exposure conditions, and other factors
may influence this relationship.
Sample size
Caution should be used in drawing conclusions when only one or a few soil
samples from a site have been analyzed. Depending on the uniformity of lead
distribution at a site, a single soil sample may significantly overestimate or
underestimate the average lead concentration at a site.
Surface soil
Because lead is immobilized by the organic component of soil, lead deposited
from the air is generally retained in the upper 2-5 centimeters of undisturbed
soil (EPA 1986). Urban soils and other soils that are disturbed or turned under
may be contaminated down to far greater depths. Opportunity for exposure is much
greater to surface soil than to subsurface soils.
Evidence for the non-uniformity of lead distribution in urban soils was
demonstrated in a study that examined soil lead concentrations in urban
Baltimore gardens (Chaney 1984). Soil lead concentrations varied more than
10-fold within a single garden.
Chemical form of lead
The impact of exposure to lead-contaminated soil on PbB levels is also
influenced by the chemical and physical form of the lead. Data from animal
feeding studies suggest that the oral bioavailability of lead sulfide and lead
chromate is significantly less than the bioavailability of other lead salts
(oxide, acetate) (Barltrop and Meek 1975).
Particle size
Increasing the particulate size also reduces the bioavailability of lead in
the gastrointestinal tract. In animal feeding studies, decreasing the lead
particulate size from 197 microns to 6 microns resulted in a 5-fold enhancement
in absorption (Barltrop and Meek 1979). The lead content of soil and dust has
also been demonstrated to vary dramatically as a function of particle size
(Duggan and Inskip, 1985). Several studies have reported that the lead content
of soil, street dust, city dust, and house dust increases as the particle size
decreases.
Lead-mining sites
The results of studies at lead-mining sites have indicated that soil lead
contamination from mine tailings may be less effective in increasing PbB levels
than is lead contamination derived from urban lead pollution (paint, gasoline)
or atmospheric lead fallout from lead smelting operations (Steele et al. 1990).
However, an animal study by LaVelle et al. (1991) on the bioavailability of lead
in mining wastes following oral intubation in young swine does not support these
findings.
The reduced bioavailability of lead from mine tailings may be related to its
chemical form (lead sulfide) and its larger particulate size. Evaluations of
mining sites require analyses of these physical-chemical parameters.
Pathways of Exposure
Soil and dust act as pathways to children for lead deposited by primary lead
sources such as lead paint, leaded gasoline, and industrial or occupational
sources of lead (CDC 1991).
Because lead does not dissipate, biodegrade, or decay, the lead deposited
into dust and soil becomes a long-term source of lead exposure for children. For
example, although lead emissions from gasoline have largely been eliminated, an
estimated 4-5 million metric tons of lead previously used in gasoline remain in
dust and soil, and children continue to be exposed to it (ATSDR 1988).
Prevention activities
Community prevention activities should be triggered by PbB levels > or =
10 mcg/dl, as recommended by the Centers for Disease Control (Table 8), (CDC, 1991).
For community-level intervention to be successful at least five types of
activities are necessary (CDC, 1991).
(1) screening and surveillance (2) risk assessment and integrated prevention planning
(3) outreach and education (4) infrastructure development (5) hazard reduction Soil lead abatement
Exposure Pathways and Populations at Risk
Soil and dust act as pathways to children for lead deposited by primary lead
sources such as lead in paint, leaded gasoline, and industrial or occupational
sources of lead. Because lead does not dissipate, biodegrade, or decay, the lead
deposited into dust and soil becomes a long-term source of lead exposure for
children.
Preschool-age children and fetuses are usually the most vulnerable segments
of the population for exposure to lead. Among children, those in the 2-3
year-old age bracket may be most at risk for exposure to lead-contaminated soil.
The number of children potentially exposed to lead in dust and soil is estimated
at 5.9 to 11.7 million children.
Uptake and Bioavailability of Lead
A strong positive correlation is found between exposure to lead-
contaminated soils and PbB levels. Generally, the PbB levels rise 3-7 mcg/dl for
every 1000 ppm increase in soil or dust concentrations. Access to soil, behavior
patterns, presence of ground cover, seasonal variation of exposure conditions,
and other factors may influence this relationship.
Bioavailability of lead in the gastrointestinal tract is influenced and may
be reduced as the particulate size of lead is increased. The reduced
bioavailability of lead from mine tailings may be related to its chemical form
and its larger particulate size. Evaluations of mining sites require analyses of
these physical- chemical parameters.
Biomarkers
The most commonly used biomarkers of lead exposure are the PbB
concentration and the blood erythrocyte protoporphyrin (EP) concentration. The
EP test has poor sensitivity and specificity below a PbB level of 25 mcg/dl. The
CDC recommends PbB concentration as the screening test of choice.
Site-Specific Exposure Assessment
Interactive and complex factors associated with multiple exposure pathways
for lead require a site-specific approach in order to develop meaningful action
levels for lead in soil. When evaluating a site, a health assessor should be
aware of multiple sources of lead exposure and the additive nature of the risks.
Dust and soil lead -- derived from flaking, weathering, and chalking paint --
plus airborne lead fallout and waste disposal over the years, are the major
proximate sources of potential childhood lead exposure.
Wide variations in soil lead levels have been reported, ranging from less
than 100 ppm to well over 11,000 ppm. Soils adjacent to houses with exterior
lead-based paints may have lead levels of >10,000 mcg/g. The downward
movement of lead from soil by leaching is very slow under most natural
conditions.
At a site, the health assessor should examine the available PbB data.
Recently, the CDC has provided guidelines for interpreting PbB test results in
children. If conditions at a site change dramatically, retesting exposed
individuals may be necessary to determine the impact of altered conditions on
PbB levels. The health assessor should pay attention to potential seasonal
variation of exposure conditions; the half-life of lead in the blood stream; and
limitations of any screening methods used, especially study design (power and
representativeness of blood and soil samples), should be evaluated.
The health assessor should use caution in drawing conclusions when only one
or a few soil samples from a site have been analyzed. Depending on the
uniformity of lead distribution at a site, a single soil sample may
significantly overestimate or underestimate the average lead concentration at a
site. The impact of exposure to lead-contaminated soil on PbB levels is also
influenced by the chemical and physical form of the lead.
ATSDR Recommendations
At all sites, ATSDR recommends that health assessors evaluate the
need for any follow-up health activities. This effort should be coordinated with
other health agencies, as appropriate, to ensure that all aspects of a site that
impact the health of the community are evaluated. The recent statement by the
CDC, Preventing Lead Poisoning in Young Children, provides guidance and
identifies community prevention activities that should be triggered by PbB
levels > or = 10 mcg/dl.
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Congress, July 1988.
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Barltrop D. and Meek F. (1979). Effect of particle size on lead absorption
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levels. May 8, 1992.
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on heavy metals in urban gardens. Agricultural Experiment Station, University of
the District of Columbia, Washington.
Chisolm JJ, Jr. (1981). Dose effect relationship for lead in young children;
evidence in children for interactions among lead, zinc, and iron. (Cited in
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Study, April 1990.
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Healy M, et al. (1982). Lead sulfide and traditional preparations: Routes for
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lead from the gastrointestinal track in humans. Hum Toxicol 1:411-5.
LaVelle MJ, et al. (1991). Bioavailability of lead in mining wastes: an oral
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Mahaffey KR, et al. (1976). Difference in dietary intake of calcium,
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To request a copy of this document or for questions concerning this document,
please contact the person or office listed below. If requesting a document,
please specify the complete name of the document as well as the address to which
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DR. CHARLIE XINTARASGeneral principles and limitations in field evaluations
Community prevention activities
determining populations at
risk and the locations of the worst exposures;
analyzing all available data to assess sources of lead, exposure
patterns, and high-risk populations; developing prevention plans;
informing health-care providers,
parents, property owners, and other key people about lead poisoning prevention;
finding the resources needed
for a successful program of risk reduction;
reducing the hazards of lead-based
paint and lead in dust and soil, particularly in high-risk buildings and
neighborhoods.
Soil lead abatement may consist of either establishing an effective
barier between children and the soil or the removal and replacement of at
least the top few centimeters of soil. Summary
References
POINT OF CONTACT FOR THIS DOCUMENT:
Agency for Toxic Substances and Disease
Registry
1600 Clifton Road MS(E-28)
Atlanta, GA 30333
E-Mail:
chx1@cdc.gov
Effects Of Inorganic Lead On Children And Adults
Soil Lead And Other Media Exposure
(Adapted from CDC, Preventing Lead Poisoning in Young Children. A Statement by the Centers for Disease Control, October, 1991. U.S. Department of Health aand Human Services/Public Health Service)
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