http://atsdr1.atsdr.cdc.gov:8080/cxlead.html -- Lawrence F. London, Jr. mailto:london@sunSITE.unc.edu http://sunSITE.unc.edu/InterGardenTitle: ATSDR - Paper: Impact of Lead-Contaminated Soil on Public Health
(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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Environmental Hazards and Committee on Accident and Poison
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The nature and extent of lead poisoning in children in the United
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Barltrop D. and Meek F. (1975). Absorption of different lead
compounds, Postgrad Med J 51:805-9.
Barltrop D. and Meek F. (1979). Effect of particle size on lead
absorption from the gut. Arch Environ Health 34:280-5.
Binder, S. and Matte, T. (1992). Personal Communication. Review
of soil lead levels. May 8, 1992.
Centers for Disease Control (CDC), (1991). Preventing lead
poisoning in young children, October 1991.
Chaney RL, et al. (1984). The potential for heavy metal exposure
from urban gardens and soils, pages 37-84. In: J.R. Preer ed.
Proceedings of the symposium 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,
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Metals Exposure Study, April 1990.
Day JP, et al. (1979). Solubility and potential toxicity of lead in
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surface dust and soil: A community problem. Public Health Rev
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EPA (Environmental Protection Agency) (1991). Three city urban
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Hammond PB. (1982). Inorganic lead in man's environment: Sources
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Harrison RM. (1979). Toxic metals in street and household dusts.
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Healy M, et al. (1982). Lead sulfide and traditional preparations:
Routes for ingestion and solubility and reactions in gastric fluid.
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Heard MJ and Chamberlain AC (1982). Effect of minerals and food on
uptake of lead from the gastrointestinal track in humans. Hum
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LaVelle MJ, et al. (1991). Bioavailability of lead in mining
wastes: an oral intubation study in young swine (submitted for
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Madhaven S, et al. (1989). Lead in soil: Recommended maximum
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Mahaffey KR, et al. (1976). Difference in dietary intake of
calcium, phosphorus, and iron of children having normal and
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Mahaffey KR, et al. (1982). National estimates of blood lead
levels: United States, 1976-1980. N Engl J Med 307(10):573-9.
Markowitz ME and Rosen JF. (1981). Zinc (zn) and copper (Cu)
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lead sources, such as house dust and hand dust, in the homes of
children. Environ Res 38:77-95.
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Steele MJ, et al. (1990). Assessing the contribution from lead in
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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 you would like it mailed.
Note that if a name is listed with the address below, you may wish
to contact this person via e-mail.
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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